Hypersensitivity microbiology notes

                         HYPERSENSITIVITY 

hello, doctor vanakam,

I hope you all are doing good, as intimated through the last post on anaerobic culture method https://www.stencildent.com/2020/08/anaerobic-culture-methods-microbiology.html if u haven't checked it out do read using this link without any further ado lets get started.

CONTENTS:

1)Definition

2)Classification

3)type 1 hypersensitivity reaction

a)1st exposure

b)2nd exposure

c)mediators of reaction

d)late-phase reaction

4)type 4 hypersensitivity

5)treatment 

1)DEFINITION:

It refers to a condition in which immune response results in excessive reaction leading to tissue damage, disease, or even death in a sensitised host.

2) CLASSIFICATION:

• Coomb and gel classification in 1963 into type 1 to 4 
• Type 1,    type 2, type 3       :

• They depend on the interaction of antigen with humoral antibodies
• They are the immediate-type reaction 

type 4 :

• They are mediated by t lymphocyte
• Delayed-type of hypersensitive reaction
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3)TYPE 1 (ANAPHYLACTIC )REACTION :

• They are involved with the IgE antibody , also called an IgE mediated type of reaction.
• The most allergic reaction
• An antigen that causes an allergic reaction: allergen
• It occurs in 2 steps: 1)first exposure (sensitization), 2)subsequent exposure

a) first exposure  

• eg)When a person inhales pollen after it enters there will be t cells against the pollen making the molecule allergen
• Allergen picked by immune cells in airways migrate to lymph node
• These are antigen-presenting cells like dendritic cells, macrophage that present to t helper cell
• When a person is allergic it exhibits co-stimulatory molecule, before t cells seize antigen is called naive t helper 
• When t cell bind to the antigen-presenting cell and co-stimulatory molecule is called primed t cell
• In type 1 it converts to type 2 cell or t helper 2, interleukin (cytokine) help in conversion IL-4,IL-5, IL-10
• B cell instead of making Ig M specific antibody it starts making IgE specific antibody
• T helper 2 also release interleukin -5 that stimulate and activate eosinophil and release a toxic substance
• Ig E specific to Fce receptor in mast cell gets attached they are called cytotrophic antibodies as they bind to  antigen surface
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 b)2nd exposure:

Few months , later during 2nd exposure , the antibody binds to an antigen they get cross-link and degranulate pro-inflammatory mediators producing an allergic reaction.

c) MAJOR MEDIATORS:

1. Histamine bind to h1 receptor resulting in bronchi smooth muscle to contract this further leads to difficulty in breathing and also because of blood vessel dilation , increase in permeability results in edema, urticaria
2. Eosinophil
3. Protease

d)late-phase reaction: 8-12 hours

Eosinophil,t helper 2 cells,and basophil are recruited to site where an allergen is located

mild symptoms are urticaria, eczema, allergic rhinitis 9inflammation in the nose , asthma

severe symptoms include increase n vascular permeability, airway constriction and may result in anaphylactic shock 

 4)TYPE 4 HYPERSENSITIVITY :

• Its a delayed type of hypersensitivity, after 48-72 hours of exposure 
• Cell-mediated response 
• immune system elements are:
• 1)Antigen-presenting cell
• 2) Major histocompatibility class 2 
• 3)Helper t cells: Based on glycoprotein present on the surface   
• a)CD4+ glycoprotein they are known as helper t cells and present MHC class 2 
• b) CD 8+ glycoprotein: they are known as killer t cells and present MHC class 1 
• phases:

1. Sensitization phase:

• When an antigen enters our body it doesn't produce any reaction unless it binds to hapten and then causes an immune response 
• When an antigen enters the body the dendritic cells engulf them and act as an antigen-presenting cell with the help of major histocompatibility complex class 2 on their surface its been recognized by cd 4 cells and t helper cell and secrete interleukin and results in proliferation of cd 4 cells.

2) Effector:

• The proliferation of cd 4 cells results in the formation of interferon-gamma and activates macrophages and release  cytokines (tumor necrosis factor, interleukin) 
• This gets activated by dd 8 cells and destroys the target organ.
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 5) treatment:

1) Antihistamine: decrease in bronchoconstriction, and vascular permeability 

2)Corticosteroids: decrease the inflammatory response

3)Epinephrine: constrict the blood vessel 

GENERAL TALK: 

Vanakam, today we have discussed about hypersensitivity reaction I would like to share my own experience on sensitivity all of us would be definitely allergic to some products like for me I am allergic to yam , turmeric I know u all might have got shocked, what? turmeric is considered to be antiseptic, how can u be allergic to it well I got your mind voice yes we do exist allergic to turmeric I googled about it in the net it was surprising to me to see that there are people with this allergic and I wasn't the only with this allergy.

UPCOMING POST  :

 The next post is about thrombosis ; definition,factors favouring thrombus formation and fate of thrombus. I hope you all understood if it had helped you do let me know in the comment section below.

                                                     thank you