This essay covers all the lecture content of lecture 1 in Immunology of Human Disease. It explores Systemic immunometabolism, in health, disease and obesity. It includes additional reading on the subject.
The first question is: Describe the alterations in the immune system when it gets activated ...
A. Describe the alterations in the immune system when it gets activated during an infection.
Elaborate on the metabolic changes that occur in response to immune activation and how
these changes support the immune response against pathogens.
Systemic metabolism and immunity are interlinked for survival. In homeostasis, metabolic
tissues like adipose tissue, muscle and liver have an anti-inflammatory infiltrate to facilitate
lipogenesis. Upon infection, acute inflammation changes adipose tissue infiltrate towards a
pro-inflammatory profile, temporarily, to provide energy to immune reactions. In this essay
we will describe the alterations in the immune system when it gets activated during an
infection and elaborate on the metabolic changes that occur in response to immune
activation and how this support the immune response against pathogens.
Metabolic tissues require macrophages to survive, they link the whole body energetics
and the immune cells. The immune cells in these tissues all have leptin receptors, important
for their immune functions and to communicate with adipokines, adiponectin, resistin and
leptin. This immune system requires high energy. Infection in lean white adipose tissues
changes the immune infiltrate towards a pro-inflammatory profile with neutrophils, Th17,
Th1 and Macrophages 1 (M1) cells. In healthy white adipose tissues, the anti-inflammatory
environment contains Th2, M2, Tregs, B cells and iNKT cells. Adipocytes during infection
secrete leptin to promote M1 development and lipolysis whereas in healthy conditions, the
adipocytes secrete adiponectin to promote lipogenesis and AMPK signalling in the M2 and
block NFkB signalling. Infected tissues will see an increased level of cytokines that promote a
temporary insulin resistance to allow a metabolic adaptation to the inflammation. These
cytokines include TNF-alpha, IL-6, IL-1beta and IFN-gamma. In healthy tissues, the cytokines
secrete anti-inflammatory IL-10, IL-4, IL-13 and IL-33. Therefore, this acute inflammation
triggers tissue protection, required for survival.
Disease tolerance, or dormancy, is activated during an infection to prevent harm to the
host. Anabolism and catabolism are triggered during this state, anabolism promoting sickness
behaviour including anorexia, social withdrawal and fatigue which is mediated by ADCYQP1+
neurons (Ilanges et al., 2022). Dormancy requires an environmental trigger which is
characterised by a divestment of non-essential functions (Wang et al., 2019). To exemplify
the importance of dormancy in infection, an experiment was conducted in mice where three
separate groups demonstrated different infection reactions and situations (Ganeshan et al.,
2019). One group of mice was kept at 22 degrees, an energetic trade-off state, and were
injected with a virus. These mice tolerated the infection even in the presence of these two
stressors. A second group of mice was kept at 30 degrees and were injected with the virus,
these mice resisted to the infection but less mice survived. A final group of mice was kept at
30 degrees without food and were injected with the virus. These mice tolerated the infection
and more mice survived, their energy was diverted to catabolism to survive. This last group
exemplified the induction of the dormancy state, where in presence of an environment
trigger, here resource scarcity, the host diverts its energy into essential functions for tissue
protection and survival.
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