#Cytokine storm

[jcrmhscasereports]

Case of Necrotizing Pancreatitis following COVID-19 Infection by Faezeh Sehatpour in Journal of Clinical Case Reports Medical Images and Health Sciences  

ABSTRACT

New aspects of COVID-19 are increasingly being recognized. Although the virus is mainly known to affect the lungs, involvement of other organs including the heart, liver, gastrointestinal, renal and pancreas is also detected. Acute pancreatitis is detected as one of both the early and late presentations of COVID -19. Cytokine storm or the presence of angiotensin-converting enzyme 2 (ACE2) receptor in pancreatic cells, are both two causes of pancreatic injury in COVID-19 infection. In this study, we reported a 25-year-old man admitted to our department with the impression of necrotizing pancreatitis concomitant with COVID-19 infection. Patient's lab data, imaging and outcomes were documented in full detail.

Abbreviations:

WBC, white blood cell;HB, hemoglobin; MCV, mean corpuscular volume; PLT, platelet; BUN, blood urea nitrogen; Na, sodium; K, potassium; ; AST, aspartate aminotransferase; ALT, alanine aminotransferase; ALK.P, alkaline phosphatase; ALB, albumin; LDH, Lactate dehydrogenase ; CPK, creatine phosphokinase; CRP,c-reactive protein; AFP,alpha-fetoprotein; CEA,carcinoembryonic antigen; CA19-9,cancer antigen 19-9; Immunoglobulin G4.

INTRODUCTION

The Covid-19 pandemic is an ongoing pandemic that started in December 2019 and spread rapidly around the word. COVID-19 was caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), first identified in Wuhan, China. So far, more than 200 countries have been affected by the pandemic. (1)

New aspects of COVID-19 are increasingly being recognized. Although the virus is mainly known to affect the lungs, involvement of other organs including the heart, liver, gastrointestinal, renal and pancreas is increasingly being reported. (2)

The involvement of the gastrointestinal system is maybe due to the expression of the angiotensin-converting enzyme2 (ACE2) on the hepatocyte, cholangiocyte and  other parts of the GI tract. (3) In a recent survey, acute pancreatitis was detected as one of both early and late presentations of COVID -19. (4-6) However, it is still unclear whether SARS-COV-2 directly affects pancreatic cells because of ACE2, if it is a cytokine storm which causes pancreatic injury. (7)

We reported a case of COVID-19 with subsequent acute necrotizing pancreatitis.

CASE REPORT

A 25-year-old man without any known medical disease presented to our emergency department with progressive epigastric pain, nausea and vomiting and anorexia one week prior to admission. He has no history of alcohol consumption. He also had a history of admission to another hospital about two weeks ago with a diagnosis of COVID-19 pneumonia. On admission, he has a blood pressure of 115/75 mm HG, a heart rate of 100 beats per minute, a temperature of 37.1 ⁰C and oxygen saturation of 95% while the patient is breathing in the room air. Primary investigations summarized in Table-1. Amylase and lipase were 146 IU/L and 82 IU/L respectively. Nasal swab test for COVID-19 (RT-PCR for SARS-CoV-2) was positive. Abdominal sonography showed markedly prominent pancreas with in homogeneous parenchymal echogenicity and large cystic lesion arising from the pancreas, in favor of acute complicated pancreatitis with pseudo cyst. The gall bladder has a normal size and wall thickness without any gall stones. The pancreatic duct was not dilated.  Due to the finding of abdominal ultra sound, CT scan of abdomen was done on him which revealed an enlarged pancreas with necrosis of the main portion of pancreatic parenchyma. Large cystic lesion measuring 15×7×11 cm in size arising from the pancreatic neck with extension to the right and left side of the abdomen suggestive of large pancreatic pseudo cyst (figure1).  Lung HRCT (low dose) also showed bilateral peripheral ground glass opacities in favor of COVID-19 pneumonia (figure2). According to the findings of a physical exam, laboratory data and clues in imaging immediate management of acute necrotizing pancreatitis (invasive intravenous hydration and pain control) was started for him. He was finally discharged from the hospital with a full recovery.

Table 1: laboratory data

Figure 1: Abdominal CT scan:  large loculated pseudo cystic structure measuring about 158mm*100mm in lesser sac due to post pancreatitis pseudo cyst formation.

Figure 2: lung HRCT: multiple ground glass and bilateral pleural effusion

DISCUSSION

Acute pancreatitis is an acute inflammation of the pancreas characterized by abdominal pain, nausea, vomiting and elevated exocrine pancreatic enzymes; amylase and lipase. Gallstones and chronic alcohol abuse are the most common causes of acute pancreatitis. Viruses are uncommon causes of acute pancreatitis. Pancreatitis has been reported with several viruses, including mumps, coxsackievirus, hepatitis A and B virus, cytomegalovirus, varicella-zoster, herpes simplex and human immunodeficiency virus. (8)

Although we have not conclusively proven the presence of the virus in the pancreas, the causes of COVID-19 and acute pancreatitis and the lack of other clear causes for pancreatitis strengthen the relationship between the two diseases.  In this study, the patient presented with necrotizing COVID-19in 19 in the early post period of COVID-19 infection.

In Fan Wang and colleagues' survey, 52 COVID-19 cases followed and showed that 17% of COVID-19 patients developed pancreatic injury and presented with mild elevated pancreatic enzymes; serum amylase and lipase without clinically severe pancreatitis. The possibility of drug induced acute pancreatitis in patients who have received medication due to COVID-19 is also expressed as one of the reasons for acute pancreatitis in COVID-for19 infection. (9) Saffa Saeed Al Mazrouei and his teammates reported a 24-year-old patient with acute non-necrotizing pancreatitis with concurrent COVID-19. No evidence of pseudo cyst or abscess was detected in his imaging. (10)

Pancreatic damage can be due to the direct effect of the virus on pancreatic cells or indirectly secondary to the immune system. In another study in Wuhan, it showed that ACE2 was expressed in the pancreas higher than the lung in the normal population, indicating that SARS-CoV-2 can bind to ACE2 in the pancreas and cause pancreatic cell damage. (7, 11)

Acute pancreatitis is one of the presentations or complications of COVID-19 infection. Further investigation with samples is needed to reveal the pathophysiology, presentation, treatment and prognosis of acute pancreatitis in COVID-19 infection.

For more information: https://jmedcasereportsimages.org/about-us/

For more submission : https://jmedcasereportsimages.org/

#COVID-19 #Cytokine storm #blood cell;HB #aminotransferase #CRP #c-reactive protein #carcinoembryonic antigen #alpha-fetoprotein #anorexia #RT-PCR for SARS-CoV-2 #HRCT #Faezeh Sehatpour #jcrmhs

[a-simple-bacterium]

I love that regulatory T cell is a spectrum of “If you even lay a finger on this cell, I will beat your ass so hard they can’t find the pieces to take you to the spleen” to “This sign says that’s a no no”

#cells at work #hataraku saibou #Lactobacillus posts #on an unrelated note #Do you think she has a button that says ‘ignore helper T cells orders’ #for whenever he goes cytokine storm mode

[chicago-geniza]

Follow an account that posts vintage eBay jackets and hats and I have never needed an accessory more than this snapback in my whole entire life

#ALLERGY 2000 #Y2K: MAST CELL MAYHEM #MILLENNIUM: CYTOKINE STORM #IgE-MAIL: Y2K AND THE CYBER ALLERGY CRISIS

[0dotexe]

There is something so deeply intriguing to me about the possibility of your impact on society being that of therapist's notes, medical observations, lab records, or possibly even a coroner's examination. Yet you, the patient, will never know exactly what these secret tomes of knowledge hold. You cannot ask for them. You cannot search your name in them. You cannot read them unobjectively. You just have to trust that even long after you've seen said practitioner, that the observations made about you will paint an accurate picture of the person they had to help in a medical setting. No matter how disturbing the tale may unfold.

⬖.Exe

#exe talkz #medical horror #sciencecore #lab records #mad science #mad scientist #lab report #i'm thinking about the TGN1412 cytokine storm incident once again

[clonerightsagenda]

Do No Harm remains a Lot to listen to in the midst of an ongoing pandemic

#'oh the virus won't kill him! the overactive immune response might do it though' #me who had to learn what 'cytokine storm' meant 3 years ago for personal reasons: #this is how i die #at least it's a strong possibility as the fuckers around me keep taking their masks off

[smol-blue-bird]

the most annoying thing in the world is Googling an immunology term and only getting 50,000 COVID articles written by non-scientists who don’t have any idea what they’re talking about in order to “educate” a population that’s relying on the news for important information about their health. The amount of misinformation is ASTOUNDING. And I don’t even mean “regular” COVID misinformation about things like Bill Gates and ivermectin, I mean misinformation generated by people who seem like they’re earnestly trying to help but who do not have ANY qualifications to be acting like an authority about virology

#trying to find ANY decent article on how hypercytokinemia leads to ARDS #I definitely spelled that wrong but. you know what I mean. #and half of the results are just people saying insane shit about cytokine storms #like man shut UP

[shoeshineyboy]

the thing with the theralizumab trial is that it’s fucking awful, and I understand that the wikipedia article had to put the quote from an anonymous writer to New Scientist in, but the quote was “you don’t need to be a rocket scientist to work out what would happen if you non-specifically activate every T cell in the body”, and that is Really Funny

#please don’t google it btw if you’re uncomfortable with pictures of injuries #find it on wikipedia instead #maybe you do need to be a rocket scientist. because the pharmacologists missed it #I am obsessed with cytokine storms and medical science and this trial is just like. my favourite article

[ricisidro]

Some of the most serious #COVID19 outcomes can result from certain viral protein fragments produced by #SARSCoV2 resembling zombie complex overstimulating the immune system, thereby causing rampant inflammation in widely different contexts such as #cytokinestorms and lethal #bloodcoagulation: UCLA study

https://newsroom.ucla.edu/releases/viral-protein-fragments-behind-serious-covid-19-outcomes

#COVID19 #sars cov 2 #Cytokine storms #Blood coagulation

[iliveinprocrasti-nationn]

normal about medicine im soooo normal about how the human body works

#chewing through metal #on one hand im so tired of fish experiments on the other hand. antibiotics #im normal im fine just don’t bring up spanish flu or tuberculosis or polio or cytokine storms or #‘j don’t u have massive trauma around disease and panic at the sound of coughing’ SHUT UP im multifasceted

[thebibliosphere]

so I’ve always had dermatographia, but since getting Covid for the 4th time this fall, I also am spontaneously breaking out on hives on my back a couple times per week. It doesn’t seem to do much, just kind of itches and then goes away after a half hour. I have no known allergies. Do you think this is indicative of some kind of mast cell issue? I can’t tell if this is an episode of weird body, meh, or a red flag of a huge impending problem.

There was a study released this year about long-covid and how it can result in symptoms similar to MCAS.

Let's see if I can find it... Ah. Here.

So, obviously, we won't know the full ramifications of covid for probably decades, but in the meantime, there is some evidence to suggest that long-covid patients show abnormal mast cell release of excessive cytokine (among other things), which is, well, when it fucks up, it fucks up.

That's what made the cytokine storms patients were experiencing in the early days of covid so dangerous. It's like the immune system equivalent of throwing napalm onto a housefire.

(I also suspect that's why so many front-line doctors now believe in the severity of MCAS. They were watching this shit happen in real-time.)

So, is it possible your recurrent covid infections have led to a bit of mast cell instability and causing spontaneous hives? Speaking anecdotally from the sheer volume of emails people have sent me and the MCAS forums now flooded with people who got covid and can't stop itching, yeah, it's possible.

But it's also possible it won't progress beyond that point.

I'd advise keeping an eye on it and talking to your doctor if you have concerns.

Also, maybe look into getting re-tested for allergies. Allergies can develop at any time in your life, and there could be another explanation for the hives.

Basically, don't panic, but do take care of yourself and watch for any other symptoms. Don't ignore any sudden new food allergies or gastro or cardio symptoms. The sooner MCAS is treated, the easier it is to manage. Mine had decades to run rampant on my body to get to the stage it was at. It doesn't have to be that way for everyone.

Take care, and I hope the hives stop!

#chronic health tag

[covidsafehotties]

Published July 31, 2023

Covid infects T-Cells directly!

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS- CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.

#mask up #covid #covid 19 #covid isn't over #pandemic #covid conscious #covid is airborne #wear a mask #coronavirus #long covid

[littlestpersimmon]

hi, I am ok rn 👍🏻 sorry for anyone I worried, I had a really bad panic attack because I wasn't sure what was going on with my body and I web'md. I was really overworked and it spiked my heart rate

In still a lot of pain and nausea, but I will head to the hospital if I don't feel better in a day or two. I talked to my nurse family member and my dad spoke to the Dr to see if this was a cytokine storm or my pcos or the possible pots. thank you to everyone who offered prayers and kind words, I feel embarrassed posting so many things but also really appreciate everyone's kindness and prayers. Thank you guys!!!!!

my cat, Faramir

[historia-vitae-magistras]

💤🤒 for Alfred please? I need to know what is so different about him.

Oh you mean my heavy-handed, pretentious idea of Alfred's increased physical abilities as a symbol of the isolating effect of American Exceptionalism? lmaooo

💤 SLEEPING SIGN — is your oc a light sleeper or a heavy sleeper? how are their sleeping habits?

Alfred sleeps! He's human; he should sleep every night, but when he doesn't, he gets along a lot better than he should. When he's excited, he won't sleep and still be fine the following day, like he got a full few hours. He can go a long time on the very minimum. He's so charismatic, and Americans are such workaholics. He can play the pied piper to overworking everyone around him as he sets the pace and tone. He will realize it sometimes, but it makes him feel weird and lonely even when he's not coked up to exceed what he can do naturally. He will start showing exhaustion, especially emotionally, but when it comes to that point, it's well past the point of breakdown. And he's a heavy sleeper. Will lay down and conk out and just trust the world not to fuck with him because there's probably a firearm within arms reach.

🤒 FACE WITH THERMOMETER — does your oc get sick easily?

Nope! This is something I've gone with since he was hatched. That he's... unusual. His standard is the human peak of health, strength, and ability, well past the point he should be. It's not entirely a benefit because an overpowering immune system might keep him sick less, but it's going to make what he does get way more miserable. See stats about how much worse the Kansas flu and its cytokine storm was in the well-fed and fresh American farm boys than in half-starved trench veterans. Shitting his brains out, delirious and with a drip in his arm, Matt's just like... slightly feverish. People who don't know him very well probably think he's being exceedingly whiny over nothing, considering the effect his economy has on theirs. He's excessively whiney about some things but good fucking god, he is not a baby when he does actually get sick. It's actually that fucking intense. When he is ill, most of the time, it's brief. He's like the kids who will have wheezing and fever of 104 at home, and then when they get to the ER, they're just a bit pale and stuffy. Matt comes down to check on him, and it's a 50/50 shot of if he's just going to be tired and kind of dehydrated but mostly okay after spending the night on the bathroom floor with the running bull of the gastro runs or burning up so bad he couldn't find the aspirin with two hands and a spotlight. He's never just had some usual run-of-the-mill shit like a cold in his life.

Character Detail Ask Game

#the ask box || probis pateo #alfred || o beautiful for spacious skies #meatsack mechanics || the sociology and biology of nations

[i-eat-worlds]

okay worlds i need your medical knowledge again.

i have a character in an apocalypse setting with no professional surgeons or doctors or hospitals in reach. they have a burn from below the left hip to the ankle, covering almost the whole leg. they have access to pharmacies, medicines and bandages, as well as five other people to care for them. i'd like the burn to be third degree, but I also need them to survive.

what is the worst degree of burn I can give them? is a skin graft possible for someone with limited medical knowledge to perform? what are the treatments, how long would it take them to get out of critical condition, and how would I ensure they survive without a professional doctor?

burn traits right now are flexible. if I can't burn their whole leg that's okay lol

thank you worlds I appreciate you <3

- @whump-kia

Thanks for the ask Kia!

disclaimer: I am not a medical professional, I’m just a nerd. Take all of this with a grain of salt. Or several.

Okay, so the severity of burns is determined by a two factors: How much skin in burned (measured by the percentage total body surface area burned. You’ll see it abbreviated as TBSA) and how deep those burns are (first degree or superficial, second degree or partial thickness, or third degree or full thickness).

The burn you’ve described (in my unprofessional opinion) would be about 18-15 % TBSA. Keep in mind that the burns wouldn’t be only third degree, their edges would be second degree, and it would sorta “fade in.”

It’s also important to take into account which areas were burned. Burns to the face, hands, genitalia, or major joints are more severe. Your injury includes a knee, which is another area of concern.

Other important things:

For a variety of reasons, burns consume a lot to fluids. Your character is at risk for dehydration and hypovolemia. In non-apocalyptic environments, they’ve be given copious amounts of IV fluids to replace what they’ve lost. This is primarily a concern in the first 24 hrs.

Hypothermia is also a concern. One of the skin’s big jobs it to insulate the body. If a large surface area has been damaged, your character will start to loose heat. They make things called “burn sheets” to help with this. They’re sterile and are designed to insulate and not stick to burns. If your character has access to a pharmacy they might have some of these.

Cytokines are a proteins that affect the immune system. They’re released when the body experiences a significant injury, like a burn. Sometimes, too many are released, causing a condition called cytokine storm. This results in feelings of fatigue and nausea, a fever, and a drop in blood pressure. This is seen around 48-72 hours after injury.

Eschar is a hardened tissue that can develop with severe burns. If the burn encircles a limb, the eschar can put pressure on the limb, cut off blood flow, and cause compartment syndrome. This doesn’t always happen-the skin can also slough off. This is sometimes called “skin slip.” I would not google photos of this unless you are brave. Infection is another big issue. Infected burns will be purulent, smell awful, and be extra painful. Burns are prone to tetanus, so I hope your characters booster it up to date. Infection can eventually lead to sepsis.

———

Treatment:

In the environment you’re in, treatment is going to consist of having your character drink lots of fluids, keeping the burn covered in clean, sterile dressings, and providing pain medication if available.

Their mobility is going to be limited, and they’re going to need help to meet a lot of their basic needs: toileting, nutrition, etc.

Without access to a hospital, there’s not a whole lot that can be done. You mentioned skin grafting, and that’s basically a hard no. It’s extremely painful, creates another open wound, and carries a high risk of infection. A surgeon doing a skin graft in this situation is unadvisable, a non-surgeon attempting this procedure is highly unadvisable. It’s best to keep them warm, hydrated, and comfortable, and keep the burns clean and covered.

———

If you want a better, more probable good outcome, I would change a couple of things. First of all, I would reduce the amount of surface area the burn takes up. Having the burns of just on the thigh and the calf would remove the knee from the equation and make the injury less severe. Furthermore, I’d make most of the burns second degree. You can have some smaller areas of full thickness burns, but second degrees will heal quicker, and, because they leave nerve endings intact, they’ll hurt more! More superficial 2nd degree burns should heal in one-three weeks, and deeper 2nd degree burn might take as many as nine weeks. If the burn takes longer than two weeks to heal, it will likely scar.

Hope this was helpful!

Sources:

Blood on the Page by Samantha Keel (cannot recommend this book enough)

StatPearls: Burn Evaluation and Management

StatPearls: Burn Evaluation and Resuscitation

Cleveland Clinic: Second Degree Burns

Cleveland Clinic: Third Degree Burns

Physiopedia: Burn Shock

#worlds babbles #ask stuff #burns #long post #injuries cw #if you’re a real medical professional feel free to add on I’m here to learn!

[giulliadella]

WE HAVE SOLVED THE MYSTERY OF WHY CELLS HATE NEUTROPHILS SO MUCH IN CAW

So, last night, my boyfriend and I got into some random discussion about programmed cell death and some new breakthroughs in medicine, you know, the usual things you talk about with your boyfriend at 1 AM. It is well known that leftover bodies of dead cells are phagocytosed (literally consumed) by macrophages. And that’s why I always wondered why aren’t cells scared of macrophages as much as they are of neutrophils, since neutrophils don’t consume the dead cells. With my limited understanding of immunity (which we technically don’t learn a lot about in biology) I thought that neutrophils only consumed invader bacteria and fungi.

And OH BOY was I wrong about that.

Because (and yes I have spent whole night researching this, I’ll provide the links to papers in the end lol) neutrophils are little freaks and not only do they phagocytose leftovers of cells they actually cause them to die in the first place. This happens during infections, especially with viruses that cause the excess release of cytokines (like Coronaviridae). Cytokines activate neutrophils who basically just follow the signal towards the infection site and there all hell breaks loose. Neutrophils phagocytose bacteria and virions (those are viruses that haven’t infected a cell yet) which is fine, but they also degranulate and NETose. I’ll explain this in simple terms to my best ability.

Degranulation is when granulocytes (neutrophils, eosinophils, basophils and mastocytes are all different granulocytes) release their granules which are kind of like little sacks inside their cytoplasm which contain various chemicals. Releasing these chemicals happens when the cell receives appropriate stimulus, the little granules expel their contents out of the cell’s interior. In the case of neutrophils, granules contain very toxic compounds that cause the formation of free radicals which damage DNA and proteins of the surrounding cells, as well as granules filled with digestive enzymes which, well, digest the surrounding tissues.

NETosis is a special type of cell death specific to neutrophils in which they literally degranulate pieces of their own, or their mitochondrial DNA together with more toxic compounds. This creates a net of DNA strands called chromatin which entangles invading bacteria and severely damages them and also marks them for phagocytosis by macrophages. But this process is not well controlled and some of that chromatin and toxic compounds can land onto neighboring cells which is, as you can conclude, very bad for them.

With these two abilities at hand, neutrophils are very well equipped to kill cells and destroy tissue. Which is good in cases when the cells are infected and the tissue is damaged, but their quite aggressive methods can damage healthy cells in the area as well, some of them will die and neutrophils will phagocytose their dead particles. 

Basically, to neutrophils every infection is a huge kill and eat all you can buffet. They literally phagocytose until they physically cannot anymore and then go to the spleen or bone marrow to die. They also allow macrophages to consume them and thus pass on the antigens for antigen presentation which influences further immune response. But they can also cause a lot of damage, especially if cytokine storm happens and they completely lose control. This is what causes SARS and it can kill you if it’s severe enough. 

Biologically speaking, neutrophils are very important because they are the first ones to come to the sight of infection and their crazy methods usually finish the things before they get too severe. They themselves produce cytokines that mobilize macrophages and dendritic cells so that more immune cells can join and help them. They also have a role in repairing the tissues they damaged.

However, other immune cells, including macrophages and killer T cells, simply don’t cause as much damage. Neutrophils just go all out, which is why they live for such a short period of time compared to their colleagues (they live for only few days, compared to macrophages who can live up to a month and lymphocytes who can live for months, even years).

So, yeah, my boyfriend and I have concluded (at 4AM this morning) that neutrophils are so feared because they damage tissue, go crazy and violently kill healthy cells by accident, then consume them and that’s not by accident, it’s a mechanism to repair tissues.

I can’t believe I wasted whole night just for this. My boyfriend is also disappointed. But I hope that we finally have an explanation for this mystery. Tell me what you think lol.

References:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8589350/

https://www.nature.com/articles/nri.2017.105

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820392/#:~:text=Neutrophils%20contribute%20to%20tissue%20injury,detail%20here%20(Kruger%20et%20al.

#cells at work #hataraku saibou #neutrophils #immunology #medicine #science #biology #i actually need help #it’s 4am

[caffeineyum]

Immune Cells if they were Halo things

CD8+ T cells: Spartans

B cells: ODSTs

CD4+ T cells: Commanders and officers

Lymph nodes: UNSC ships

Organs: UNSC planets

Neutrophils: Marines

Macrophages: Planet side militias

Dendritic Cells: AI

Halo rings: Cytokine storm

The Flood: Roided out cancer or tuberculosis

#immunology #immunology shitpost #halo shitpost #halo