Recommendable! This is a reminder that our natural immune system is very imperfect and needs improvement!
"Even after prevailing over a viral infection, our immune system stays active, protecting us from any lingering viruses or recurring disease. But what happens if we pick up a bacterial infection – say, salmonella food poisoning from take-away chicken soup – while recovering from flu or COVID-19? A new study at the Weizmann Institute of Science published today in Immunity, shows that in such cases, the immune system has a clever way of setting priorities, one that might be exploited for the development of future therapies against autoimmune diseases. ...
This means that innate and adaptive immunity generally come to the fore at different stages of an infection. But when one infection is followed by another ... the two arms are forced to go into high gear at the same time ...
they found that the interaction ends in a clash: Infection with [disease A] interferes with the manufacture of antibodies against the [disease B]. In other words, when faced with a lethal threat, the immune system shuts down mechanisms needed for long-term protection, dealing instead with the more urgent danger. ...
Most immune cells adapt to this shortage by changing their metabolism, shifting to burning glucose for energy instead of oxygen. But for a subset of B cells that reside in the lymph nodes in microscopic structures called germinal centers, an oxygen shortage proves fatal: Unable to adapt their metabolism, these B cells choke and die. This is precisely the subset of cells that plays a key role in adaptive immunity, generating antibodies having the best possible fit against the invading pathogen. The death of these cells puts an end to the production of antibodies required for long-lasting protection against the viral infection. ..."
This means that innate and adaptive immunity generally come to the fore at different stages of an infection. But when one infection is followed by another ... the two arms are forced to go into high gear at the same time ...
they found that the interaction ends in a clash: Infection with [disease A] interferes with the manufacture of antibodies against the [disease B]. In other words, when faced with a lethal threat, the immune system shuts down mechanisms needed for long-term protection, dealing instead with the more urgent danger. ...
Most immune cells adapt to this shortage by changing their metabolism, shifting to burning glucose for energy instead of oxygen. But for a subset of B cells that reside in the lymph nodes in microscopic structures called germinal centers, an oxygen shortage proves fatal: Unable to adapt their metabolism, these B cells choke and die. This is precisely the subset of cells that plays a key role in adaptive immunity, generating antibodies having the best possible fit against the invading pathogen. The death of these cells puts an end to the production of antibodies required for long-lasting protection against the viral infection. ..."
From the abstract:
"Consecutive exposures to different pathogens are highly prevalent and often alter the host immune response. However, it remains unknown how a secondary bacterial infection affects an ongoing adaptive immune response elicited against primary invading pathogens. We demonstrated that recruitment of Sca-1+ monocytes into lymphoid organs during Salmonella Typhimurium (STm) infection disrupted pre-existing germinal center (GC) reactions. GC responses induced by influenza, plasmodium, or commensals deteriorated following STm infection. GC disruption was independent of the direct bacterial interactions with B cells and instead was induced through recruitment of CCR2-dependent Sca-1+ monocytes into the lymphoid organs. GC collapse was associated with impaired cellular respiration and was dependent on TNFα and IFNγ, the latter of which was essential for Sca-1+ monocyte differentiation. ..."
Bacterial infection disrupts established germinal center reactions through monocyte recruitment and impaired metabolic adaptation (no public access)
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