Discuss the acute inflammatory response and its importance in controlling infection.

 Inflammation is a stereotypic, non specific response to infection. Its functions are to:
·         Deliver components of the immune system to the site of infection
·         Eliminate pathogen (if present)
·         Repair the damage
·         Return to homeostasis

Ideally the inflammatory response should be rapid (acute), destructive, but also localised and self limiting.
This essay will describe the events that occur during the acute inflammatory response and discuss its importance with respect to controlling infections.
Inititaition/trigger
The initiation and/or trigger for the acute response is the afferent arm of the immune system. Its function is to detect dangerous stimuli (which include PAMPs but also ‘self PAMPs’) and subsequently trigger the acute inflammatory response. This serves to either resolve the stimuli or recruit the adaptive immune system to deal with the stimuli.
The mechanism by which this occurs is as follows:
PAMP -> PRR ->Upregulation of cytokine triggers for effector function
PAMPs are broad pathogen specific molecules that are generally not found on the host cells and serve to allow detection of ‘harmful’ from ‘harmless’. These may include mannose, fuccose, flagella, dsRNA, etc.
These are detected by PRR. The main is TLRs which are specific for different types e.g TLR 4 flagella etc. There are also other PRRs such as MBL (which forms part of complement pathway, mentioned later) but also Cytosolic NOD like receptors as well.
These, via NFkB cause the upregulation of proinflammatory cytokines such as IL-1, IL-2 TNFalpha.
Recruitment of effector function
In order to resolve the situation, effector function is required. In the case of the acute inflammatory response this is mainly achieved by neutrophils and also complement (described later). The process of the recruitment is mediated by cytokines.
Firstly the release of cytokines such as TNF alpha cause vasodilation and also increased permeability of the vessels. This results in the stereotypic ‘hallmarks of inflammation – calor, tumor and rubor’, it serves to increase bloodflow and allow for more leucocytes to reach the area. (note dolor – pain may also be caused by cytokines acting upon nociceptors and serves as a signal to protect the injured or infected body part by causing increased sensitivity).
The cytokines also cause upregulation of adhesion molecules such as selectins and integrins which allow the recruitment of leucocytes across the vessel wall:
Draw diagram for rolling tight adhesion diapedesis chemotaxis
Make sure to mention specific molecules selectins P and E to sialy lex.
Integrins ICAM1 – LFA1
Diapedesis CD31
After diapedesis cytokines also act as chemotaxins for the movement of neutrophils. This movement occurs by cytoskeletal rearrangements.
Effector function: Leucocytes and complement
Leucocytes in the area
The principal leucocyte for acute inflammation is the neutrophil macrophages are also involved. Once in the area it will phagocytose the pathogens and will kill it by the fusion of a phagosome with lysososme to cause the production of a phagolysosme which contains ROS and lytic enzymes such as lysozymes.
Note if these pathogens are not dealt with, it can result in chronic inflammation which can cause local bystander damage
Complement
Another aspect of the immune system is complement. These are several proteins in the serum produced by the liver. They were initially named because it was a property that ‘complemented’ the action of antibodies up to 56 degrees Celsius
Now it is established that it actually acts almost as an independent system as it has its own mechanisms of detection and effector function. However it has some key interactions with other aspects of the immune system.
Draw diagram.
Describe selectivity – cd59 daf mcp etc.
Resolution
Ideally, the acute inflammation manages to deal with the infection and the healing process can begin. This includes the phagocytosis of debris by macrophages. Also the expressions of cytokines IL-12 and TNFa as well as FGF and VEGF. Thiss allows for the recruitment of fibroblasts which produces collagen and other ECM proteins. It also allows for angiogenesis as well.

Note if inflammation continues while this processing is occurring it is no longer acute inflammation but is referred to as chronic inflammation.
Originally written by Georgia Winter

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