Question

Describe the processes associated with inflammation. What chemicals and cells are involved? What are the hallmarks of inflammation? Describe hypersensitivity and each category of hypersensitivity.

Answer 1

Describe the processes associated with inflammation. What chemicals and cells are involved? What are the hallmarks of inflammation?

The process of inflammation & chemical and cells are involved:

Inflammation process:

1. Vasoconstriction: It has vital importance to regulate the “blood loss at the time of injury” & inflammation therefore, platelets will be activated

2. Vasodilation: this is followed by initial vasoconstriction where higher number of erythrocytes are accumulated at the site of injury result in increase with fluid leaves blood vessels

3. Formation of edema due to higher exudate in tissue

4. Migration & diapedesis: polymorpho nutrophils and leukocytes are going to migrate at the region of vessel walls

5. Degranulation: release of inflammatory and pro-inflammatory factors such as histamine and Prostaglandins at the site of inflammation result in increased permeability finally increased leukocytes to reach extracellular space

6. The other blood cells and proteins are going to migrate into tissue where there will be control on inflammation by activity of immune system in which cells such as phagocytes act in the area to clean debris

8. Stimulation of plasma systems to produce the clot

Hallmarks of inflammation: Both acute & chronic inflammation is associated with infiltation of mononuclear cells and followed by fibroblast formation result in fibrosis in connective tissue finally tissue destruction occurs

Initiation of inflammation: Bacterial antigens are going to bind with antigen presenting cells finally taken by the macrophages, B-cells, or T-cells after initiating immune response. The inflammatory mediators are secreted during phagocytosis are cytokines, interleukins trigger inflammation as they are the inflammatory mediators

For example:

The main immunological inflammatory factors that were involved in tonsil swelling as follow. The Toll like receptors (TLRs) are signaling receptors, and their activation leading to enhancement of the antimicrobial activity of macrophages and neutrophils result in the generation of cytokines predominantly by macrophages at the site of infection followed by TLR s activation to present antigen to naïve T cells. This process of macropinocytosis (microbial engulfing) occur through TLRs that induces the dendritic cells maturation finally cell migration to the lymphoid organs (tonsils) where they defend and stimulate antigen-specific T cells to produce cluster differentiation molecules such as CD40, CD80 to act against infection via endosomal pathway.

In case of viral tonsillitis, these same activated T-cells generate chemokines and cytokines to enable adaptive immunity including pro-inflammatory cytokines tumor necrotic factor (TNF-aplha) that generate mild fever followed by interleukin-1, IL-6 and IL-12 whereas dendritic cells, plasmocytoid dendritic cells generate antiviral interferons I (INF α, INF β) in response to viral tonsillitis.

Ques-2: Describe hypersensitivity

Desensitization is the process of rising the dosages as if the antigen is injected beneath the epidermis of skin thereby finally result in delivery of immunoglobulin G (IgG) instead of immunoglobulin E (IgE) antibodies. These immunoglobulin G antibodies are going to bind with antigens inside the body leading to agglutination result in hypersensitivity reactions. Finally this IgG is going to interact with cell bound IgE leading to anaphylactic systemic shock that spreads entire systemic circulation. The predominant desensitization induced mechanism involves that if IgG is going to bind to IgE of polynuclear granulocytes (circulating basophils) thereby releasing inflammatory mediators such as granzymes in the systemic circulation further result in blood vessel dilation.

Delayed hypersensitivity:

IgE antibodies are released more during allergic conditions; they trigger the body’s reactivity towards the foreign particles. During heyfever, histamines are released from the mast cells, which is a major component of hypersensitivity reactions.

Hypersensitivity reactions produced by the plant mitogens such as pokeweed, phytohemagglutinin and concanavalin A. Bacterial products such as exotoxins and endotoxins are superantigens normally at physiological conditions at appropriate temperature and PH, attacks host cells followed by activation of naïve T cell clonal proliferation as well as phorbol esters. Bacterial toxins are lipopolysaccharide molecules. Host physiological condition favors them for their growth and they presented by antigen presenting cells to T cells. T cell proliferation follows a variety of signals due to T cells Toll like receptor engagement with bacterial exotoxin or mitogen (antigenic ligand) result in stimulation of gene expression to produce cytokines including synthesis of DNA for cell division. This is result in mitogen-induced lymphocyte proliferation during cell –mediated immunity with the following events.

Type I & type II hypersensitivy reaction:

Systemic lupus erythematosus usually due to autoimmune disease and due to Type II and II hypersensitivity reactions in the body result in butter fly shaped reddish clinical manifestations on the skin due to photosensitivity.

Type IV hypersensitivity reaction: Delayed Type T Cell-mediated hypersensitivity (DTH)

Two predominant immune-modulators involved in Type IV hypersensitivity reactions are – Cluster differentiation CD4 -TH1 cells and CTL

Sensitization phase: In this phase the foreign antigen is processed (Via APC/major histo- compatability -II ) and exposed to the TH-1 cells there by transformation of TH0 TH-1 cells.

Elicitation phase: In this phase, immunomodulators and immune chemical mediators such as cytokines, chemokines released upon re-exposure of the effector TH1 cells meticulously to the sensitizing antigen and finally result in activation of the macrophages (inflammatory response). These chemical mediators released by the cells are Interferon gamma, macrophage chemotactic activating factor with associated inhibition factors.

Delayed hypersensitivity reaction (DTH) is mediated by the activation of the monocytes (mononuclear leucocytes) and macrophages in association with Cluster differentiation CD4 -TH1 cells and CTL cells finally result in an inflammatory response. These reactions not mediated by antibodies.