#phagocytose

[lxikoniko]

Who's winning: 2145 or 4989

#cells at work #hataraku saibou #2145 is constantly eating more often but is said to do it in a workaholic way #4989 would phagocytose his own body if he could #both idiots in very different ways #the absolute absent minded look in both of their eyes give off completely different vibes

[redconsumerism]

TO CONSUME IS (not) TO LOVE

cannibalism in romance novels

Cannibalism is like a parallax. For once it exists as a ‘philia’, characterized by the desire of eating another. And we find that it exists in the opposite spectrum, in the form of a ‘phobia’, which speaks of the fear of being eaten or partaking unknowingly or forcefully in the act of eating another. To vore is adjacent to love in most cases, both feared and desired. Because to love someone is (apparently) to want to consume them. 

Though cannibalism might seem like a barbaric and horrific concept, it is said to be one of the most intense demostrations of love that exist in both classic and contemporary literature. The gruesome gesture reminds the lecturer of the intensity of love and its lunacy. As Mercedes Abad stated in spanish newsletter ‘el tiempo’ on May 21st, 1995 ‘There is no doubt that love and sex are feasts where, to a greater or lesser extent, we all become anthropophagi who would surely find it quite difficult to answer the question of whether there is greater pleasure in phagocytosing the other or in being phagocytosed.’ Because Cannibalism as a metaphor for love in romance novels, as it is in our day to day, is more about the blind consumerism of it rather than the pureness of it. One example of blind consumerism of love would be in Salvador Dali's Autobiography, where it is mentioned how Gala cooked their pet rabbit because of how much they loved it, in front of the woman’s refusal to the idea of leaving the rabbit with the maids.

To love is to consume, but to consume is to devour and transform in reusable energy. Like a vampire would when consuming someone’s blood, so they can continue living at the other’s cause. You live off the love you take, but if you devour that love, the other cannot live. The truth is cannibalism has a double connotation, and consuming the other’s otherness is three dimensional. Which means it isn’t always about love, or the lack thereof, but more so about the act of possessing. Cannibalism isn’t only one of the greatest manifestations of tenderness (for many), but also the irrevocably selfishness of an individual blinded by desire - in front of the morbid contemplation of the lover giving themselves so the other can survive -. The amorous-sexual instincts that resurface from a deep sense of infatuation together with those of hunger - a basic instinct - that create an irrational longing, unite in cannibalism as an analogy for that which we wish to become one with. It leaves you to question if the love narrated is but an act of survival for starved people.

‘Love is only a prologue to two cannibals struggling to take a bite of each other.’ - La Oscuridad, Ignacio Ferrando Perez (2014.) Cannibalism is, then, the imposture of love, and the obscure craving of something bigger than yourself without any understanding of it. 

#canibalism #cannibalistic #cannibalism as a metaphor for love #cannibalism is the imposture of love #love #romance #classic literature #literature #analysis #mataphors #analogy #books #books and reading #my take on cannibalism #art is subjective

[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

[centers-for-disease-control]

Hi!!! You help control diseases, right? I need advice! So I’m a macrophage, and earlier today I phagocytosed some bacteria I found near the intestinal epithelium. I thought I would be able to get rid of them no problem, but for some reason I can’t seem to kill them??? They’re just sitting there in my phagosome just—aaaaaaaah, I think they’re starting to divide now! Help!!!

Have you asked them to not?

#centers for disease control

[a-simple-bacterium]

Betting you guys do make a White blood cell list based on how much they actually seem to enjoy consuming the bacteria. All major wbcs. The main criteria is this:

1. Do they enjoy the taste of what they phagocytose (displayed by either facial expression or vocalizing it)

2. How often do they phagocytose?

3. Do they see it as a benefit of free meals or rather a duty to be done?

4. Vibes

You have 3 years. Don’t disappoint me

#cells at work #hataraku saibou #lactobacillus posts

[heckthis-heckallofthis]

I still can’t get over Mast cells being about to phagocytose. Imagine just being some cell near the skin with some dead bacteria killed by histamines or something and then just some cell, not even a white blood cell or monocyte is just like “oh, I got it :)” and then just eats it but way sloppier than a professional phagocyte.

Oh man Mast cells can phagocytose? I can imagine the Main's mast cell being embarrassed to do it in front of people, despite her enjoying the taste of bacteria. I like taking things that are in real life and applying them to our cells, send me more of these.

#cells at work #hataraku saibou #ask #asks #anon

[sergeantnarwhalwrites]

Hiya!

Do you believe in aliens? 

Do you prefer dogs or cats? 

Hey!

I do! But not like stuff on the level as us or above. That takes a long time. XD The science nerd has been cracked open a little. Archaea and Prokaryotic organisms should still count as alien life forms. So basically molds and bacteria. I'm sure there's plenty of wild archaea vibing in hellish environments and protists ready to be phagocytosed.

Dogs for sure. Mostly because I know more about dogs than cats. So it's just a comfort thing because I like both.

#thanks for the asks!

[toklabou]

浅井ゲルマニウム研究所の安積さんたちとの共著の論文が International Journal of Molecular Science オンラインで公開されました。

#Ge-132

[jhavelikes]

Chimeric antigen receptor (CAR) T cell therapies have successfully treated hematological malignancies. Macrophages have also gained attention as an immunotherapy owing to their immunomodulatory capacity and ability to infiltrate solid tumors and phagocytize tumor cells. The first-generation CD3ζ-based CAR-macrophages could phagocytose tumor cells in an antigen-dependent manner. Here we engineered induced pluripotent stem cell-derived macrophages (iMACs) with toll-like receptor 4 intracellular toll/IL-1R (TIR) domain-containing CARs resulting in a markedly enhanced antitumor effect over first-generation CAR-macrophages. Moreover, the design of a tandem CD3ζ-TIR dual signaling CAR endows iMACs with both target engulfment capacity and antigen-dependent M1 polarization and M2 resistance in a nuclear factor kappa B (NF-κB)-dependent manner, as well as the capacity to modulate the tumor microenvironment. We also outline a mechanism of tumor cell elimination by CAR-induced efferocytosis against tumor cell apoptotic bodies. Taken together, we provide a second-generation CAR-iMAC with an ability for orthogonal phagocytosis and polarization and superior antitumor functions in treating solid tumors relative to first-generation CAR-macrophages.

A second-generation M1-polarized CAR macrophage with antitumor efficacy | Nature Immunology

[thebrokencrescent-blog]

📆 Aug 2019 📰 Penetration of CD8+ Cytotoxic T Cells into Large Target, Tissue Cysts of Toxoplasma gondii, Leads to Its Elimination

Toxoplasma gondii is an obligate intracellular protozoan parasite that can establish a chronic infection in humans. One-third of the human population in the world is estimated to be infected with this parasite. The basis of the persistent chronic infection is the cysts, which can contain hundreds to thousands of bradyzoites surrounded by the cyst wall, in various organs, especially the brain. This chronic infection can reactivate in immunocompromised individuals, such as those with AIDS, neoplastic diseases, and organ transplants, resulting in life-threatening toxoplasmic encephalitis. Even in immunocompetent individuals, recent epidemiologic studies shed light on the pathogenic effects of this widespread chronic infection by reporting a higher incidence of multiple types of cancers in individuals seropositive to this parasite. Current chemotherapy is effective only against tachyzoites.

We investigated how CD8+ T cells remove tissue cysts of Toxoplasma gondii, which can grow to the size of >50 μm in diameter within infected cells. Notably, immunohistologic analyses in the brains of infected mice visualized the presence of numbers of CD8+ immune T cells that had migrated halfway through the cyst wall as well as T cells located fully within the cysts. Perforin was required for their invasion and cyst elimination. Cysts invaded by the T cells displayed morphologic deterioration and destruction. Within these deteriorated cysts, granular structures intensely positive for granzyme B were detected in association with T. gondii bradyzoites.

Furthermore, the bradyzoites within the destroyed cysts were located within accumulated ionized calcium binding adaptor molecule 1 (Iba1)-positive microglia and Ly6C+ macrophages, suggesting that these phagocytes had phagocytosed those organisms for their eradication. The present study uncovered a previously unappreciated capability of CD8+ cytotoxic T cells to penetrate into a large target, T. gondii cysts, their elimination. This invasive capability of CD8+ cytotoxic T cells in collaboration with phagocytes appears to be a powerful effector mechanism that functions against not only T. gondii cysts but also other large targets, including solid cancers.

[fahneditor]

The Innate Immunity Defense against Gastrointestinal Nematodes: Vaccine Development

The nematode parasite infects both humans and animals, causing severe infections. Their unusual surface structures, in particular, pose significant challenges to the immune system. Vaccine-induced immunity, mediated by the innate immune system, could be crucial in the development of an adaptive effector response. The purpose of this paper was to provide an overview of recent research on the host’s innate immune system, barriers, and cells that respond to parasitic nematodes. This study investigated the nematode-associated molecular patterns that may recognize by the host. Given that innate defense is more than just a static barrier against pathogen infections. It can actively contribute as a director of the adaptive immune response, which is ultimately responsible for the rejection of invasions. Some nematode parasites can actively move through tissues, and they pose a challenge to the innate immune system. Furthermore, their cuticular surface, which varies with each molting, cannot be phagocytosed. The nematode’s thin, carbohydrate-rich surface layer, as well as the chemicals produced by this layer, cause the first contact with the host’s innate immune system. It can be concluded that all components of the innate immune response can be activated and play an important role in the adaptive immune effector response.

#cows #sheep #immune system #parasite #veterinary #vaccine

[a-simple-bacterium]

Myleocytes being able to phagocytose is so funny to me. How did they teach those babies to eat?

[system-of-cells-interlinked]

I was listening to Continuum by Opeth, and of course I've already thought about its lyrics, but I don't think I've ever put my thoughts on paper, so here it goes.

My interpretation of this song is that it is about looking at what things are and not necessarily rejecting or disliking this present, but nonetheless regretting all the things that didn't ever get to be and the things that you know won't be.

Life is so fragile, I know And even if I heard A yearning voice in your heart Old routines always kept us apart The river of time flows on Blind and ruthless

I think the most heartbreaking line in any song ever is "The river of time flows on blind and ruthless" in this song. That line fucking gets to me every time. It is such a final statement, heavy with the weight of inescapebality.

That entire last verse, actually, is perfect. It speaks to me on a personal level. I don't think [kept us apart, or the entire song] it's about a person specifically, though it could be, but about all the things we yearn to do and don't, for one reason or another (some legitimate, some not). About all the callings we don't hear or we don't answer. It's about regret and knowing we will do things we regret, but that's life. It's about realizing, at one point in life, that time is going far away from us. Goes hand in hand with these lines from earlier in the song:

Once there was a moment Time was on my side

Because up until a point we live withouth the awareness that time is leaving us behind, that it's escaping through the crevices and that we'll never get it back. And at one point realizing that is like a punch to the gut, it puts things on a new perspective.

It makes one realize that no matter what they do, and how much they win, they are also losing.

And in that dance with time, we change, but it all stays with us, everything we've ever been and aren't anymore, everything we will be. This continuum, this sequence of people who we've been and who we've became and who we will be. It's all the same and not, at the same time. Sometimes living is just phagocytosing what we are now to become someone different in the future, and it's inevitable that parts of ourselves get destroyed in the process, even if we would like to keep them.

A part of our past is still there Underneath your shoes The memory's stuck in your chest The idle truth is up to you The river of time flows on Blind and ruthless

And maybe sometimes we promise ourselves that things will be different. Maybe we will try to keep all those version of ourselves existing, making up a coherent human being.

But that's not how it goes, because that kind of promise never works:

You are moving away from home Escaping the monochrome One after another Striding along the road Past the crest, you will be free Laid to rest now, let it be Honest promise to a degree The edge too sharp for guarantees

And the river of time flows on blind and ruthless.

#today i woke up and decided to have an existential crisis #i'm just very captivated by this song #opeth #continuum #in cauda venenum #music #personal post

[leedsomics]

Use of an Integrated Multi-Omics Approach To Identify Molecular Mechanisms and Critical Factors Involved in the Pathogenesis of Leptospira

Leptospirosis, a bacterial zoonosis caused by pathogenic Leptospira spp., is prevalent worldwide and has become a serious threat in recent years. Limited understanding of Leptospira pathogenesis and host response has hampered the development of effective vaccine and diagnostics. Although Leptospira is phagocytosed by innate immune cells, it resists its destruction, and the evading mechanism involved is unclear. In the present study, we used an integrative multi-omics approach to identify the... http://dlvr.it/SkTmQC

[kragelundrutledge49]

CGI-58: Versatile Regulator regarding Intra-cellular Lipid Droplet Homeostasis

These types of study efforts get often already been related regarding the guns which discover a new pick mobile population are regularly examined to ascertain their own term inside cellular material regarding distinctive organs/tissues. On this evaluate, we are going to increase the actual state of investigation including decide on tissue-derived come cellular numbers such as the liver organ, central nervous system, as well as cardiac tissues as examples of the accomplishment along with difficulties of this type associated with research. Last but not least, the difficulties of scientific remedies will probably be talked about because it pertains to these kind of distinctive mobile numbers learn more .Regardless of demanding treatment method, steroid-resistant nephrotic malady (NS) typically moves on to be able to end-stage renal disease. Therefore, a far more accurate and quick histological analysis is necessary to properly deal with this kind of individuals. The goal of this study ended up being to introduce a singular procedure for the histological diagnosing child NS simply by lower vacuum encoding electron microscopy (LVSEM) and to identify your morphological variations in glomeruli in between steroid-sensitive and steroid-resistant NS types. The individuals were about three sufferers using steroid-sensitive NS and 4 individuals along with steroid-resistant NS. Typical renal biopsy paraffin areas had been tarnished with platinum-blue (Pt-blue) or even routine acid methenamine silver (PAM) and immediately observed underneath LVSEM with magnifications among x50 along with x 10,Thousand. The Pt-blue-stained portions confirmed three-dimensional structural adjustments to glomerular podocytes as well as foot processes. PAM-stained sections demonstrated modifications in the framework and breadth with the glomerular basement tissue layer (GBM). Therefore, several round-shaped podocytes as well as spear like primary base procedures ended up solely regarded throughout steroid-resistant NS, despite the fact that irregularities throughout ft . course of action interdigitation, fusions, effacements, and also microvillus alterations were noticed in both steroid-sensitive along with steroid-resistant NS. Problems in thickness as well as the wrinkles involving GBMs were clearly detected inside steroid-resistant NS. Your examination by LVSEM might be ideal for the actual kidney histological diagnosis of kid NS.Coxiella burnetii is an obligate intracellular Gram-negative virus. A distinctive characteristic involving D. burnetii will be its capacity to reproduce within citrus phagolysosomes; nonetheless, the components utilized in evading web host safeguarding usually are not effectively outlined. Here, we investigated human neutrophil phagocytosis associated with H. burnetii (Eight Kilometer, phase 2; NMII) as well as the effect of phagocytosed creatures on neutrophil sensitive o2 species (ROS) creation. All of us learned that opsonization with immune system solution considerably increased phagocytosis of NMII Man neutrophils phagocytosing opsonized NMII created hardly any ROS in comparison with cellular material phagocytosing opsonized Staphylococcus aureus, Escherichia coli, or zymosan. Nevertheless, phagocytosis involving NMII failed to get a new future ROS reaction to a new disolveable agonist, suggesting hang-up had been localized on the phagolysosome and it was not a worldwide result. Certainly, evaluation regarding NADPH oxidase set up in neutrophils following phagocytosis established that translocation of cytosolic NADPH oxidase proteins, p47(phox) and also p67(phox), towards the membrane ended up being lacking in cellular material phagocytosing NMII, as compared to cellular material phagocytosing Utes.

#Kinase Inhibitor Library #HDAC inhibitor #Tomivosertib #E-64 #Geldanamycin #Molidustat #SGC-CBP30 #Dynasore #UNC0642 #Halofuginone #Avasimibe #Fasudil #Thymidine #BAPTA-AM #Fimepinostat #AP-III-a4 #CFI-400945 #PF-8380 #BMS-1 #kira6 #Aspirin #Vancomycin #Amiloride #lurasidone #Dexmedetomidine #Raloxifene #Menadione #Tolvaptan #Thiotepa #Grazoprevir