In several clinical settings such as pancreatitis and trauma, a secondary infection can be frequent and often causes death. I wonder if the body in a hyperactivated status would amplify the detrimental effect of bacterial infection. Is there any literatures on this aspect?
- There are two phases of responses one preparatory and active phase. When primary infection takes place body take every thing selectively in account and start counter action against the pathogen either by any mode innate defense, cell mediated and humoral immune defense. But when secondary infections mainly of nosocomial origin they never remain on route the bone marrow and spleen, and T helper cells could not find them in blood stream, they skip out the action of macrophages very cleverly, in addition major action of cell mediated immunity is also foiled by the bacteria by sitting locally inside the glands or inside particular organ. These pathogens multiply enormously, and their antigens are not remain presented to the APCs antigen presenting cells, therefore no antibody is synthesized and long range defense is foiled that is much enough for resurgence of microbial pathogen.
Mechanism in the prevention of autoimmune diseases describes shortly: in the human adaptive immune system T cell-mediated immunity is under modulatory control of the active 1,25-(OH)2D3, which causes T-cells to go towards T helper type 2 (T2) instead T1. Vitamin D3 is one of the several factors to form the microenvironment inside the dendritic cells to induce regulatory T cells. Vitamin D3 seems to play an important role in mediating immune function via numerous pathways, e.g. the cathelicidin and defensin are furthermore chemotactic to neutrophils and T cells activating so the dendritic cells. Because vitamin D3 plays such a critical role in activating the body’s immune system e.g. against autoimmune and infectious diseases, it is important to have vitamin D3 supplemented optimally from the birth on.
I think it is true. The second immune challenge,such as LPS or injure, indeed exert more harmfully than the first stimulation only. Here is an article based on animal models. The PMID: 16135757. Good luck!
I agree with you. But I can not follow the third explanation. Do you mean the second challenge damage the immune tissue or organs? Such as, altering the total number of T cells or subgroups. I am reasrching the effect of influenza vaccination on cognitive function during pregnancy. And i have found A(H1N1) influenza vaccine vaccination contribute to neurogenesis in offspring and pregnant mothers. I think the mechanism links to T cells in the periphery, such as the systemic T cells were recruited to the choroid plexes.
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