Acute inflammation- cellular events

During phagocytosis, NADPH oxidase and myeloperoxidase work together in killing bacteria. NADPH oxidase, located in the leukocyte cell membrane gets activated and reduces oxygen from the surrounding tissues to superoxide. This is known as the “respiratory burst”.

Ans. is ‘b’ i.e., Opsonisation

Opsonization

.   The coating of an antigen or particle (eg. infectious agent) by substances such as antibodies, complement components and fibronectin facilitate phagocytosis.

1. Antibody alone acts as opsonin
2. Antibody plus antigen can activate complement via classical pathway to yield opsonin.
3. Opsonin may be produced by a heat labile system in which immunoglobulin or other factors activate C₃ via alternative pathway.

Opsonin

.   A substance capable of enhancing phagocytosis.

.  Antibodies and complement are the two main opsonins.

About other options:

.  Cross reactivity

Some times single antigen stimulates production of variety of antibodies that more or less resemble the correct fit for the antigen. Each of these antibodies may attack different antigens that more or less resemble one another. This is known as antigen cross reactivity.

.   Immunological tolerance

Immunological tolerance is the condition in which contact with an antigen specifically abolishes the capacity to mount an immune response against that particular antigen when it is administered subsequently.

.  Immunological surveillance

It is the process by which cell mediated immunity destroys malignant cells that arise by somatic mutation.

Ans. is ‘d’ i.e., C3b- Fc mediated destruction

• Here, the examiner is simply asking about the opsonization. Complement (especially C3b) and Ig coating the bacteria act as opsonin and enhance phagocytosis.
• The speed of phagocytosis can be increased markedly by bringing into action two attachment devices present on the surface of phagocytic cells

i)        Fe receptor :- which binds the Fc portion of antibody molecule, chiefly IgG

ii)      Complement receptor (CR3) :- which binds the third component of complement especially C3b.

• This coating of the organisms by molecules that speed up phagocytosis, is termed `opsonization’ and the Fc portion of antibody and C3b are termed as opsonins.

Now the question crops, how does opsonins enhance phagocytosis : ‑

• Both the membrane of a phagocytosing cell and its target have a negative charge (zeta-potential), making it difficult for the two cells to come close together. Once the opsonins attach to the target, the negative charged is masked. Take note that the negative charge of the target doesn’t disappear. The opsonin simply overrides the charge, making it easier for white blood cells (phagocytic cells), to undergo phagocytosis. During the process of opsonization (also, opsonisation), antigens are bound by antibody or complement molecules. Phagocytic cells express receptors, CR1 and Fc receptors, that bind opsonin molecules, C3b and antibody, respectively. With the antigen coated in these molecules, binding of the antigen to the phagocyte is greatly enhanced. In fact, most phagocytic binding cannot occur without opsonization of the antigen.
• Furthermore, opsonization of the antigen and subsequent binding to an activated phagocyte will cause increased expression of complement receptors on neighboring phagocytes.

About option c

• As you all know, inside the phagocytes, bacteria are destroyed by lysosomal enzymes (lactoferrin, lysozyme
  defensins) and reactive oxygen intermediate (myeloperoxidase system, superoxide, H₂0₂, hydroxy radicals).
• However, this process has nothing to do with opsonins. Opsonins enhance phagocytosis by masking the negative charge on the bacterium so that it easily comes in contact with phagocytes.

Ans. is ‘a’ i.e., Opsonisation

 The coating of an antigen or particle (eg. infectious agent) by substances such as antibodies, complement components and fibronectin facilitate phagocytosis.

Ans. is ‘a’ i.e., NK cells

Natural killer cells destroy cancer and viral infected cells.  They are considered part of nonspecific resistance because they generate the same response to any damaged cell and do not lead to antibody production or immune system memory.

Ans. is d i.e., Decreased hydrostatic pressure

Acute inflammation is characterized by marked vascular changes, including vasodilation, increased permeability and increased blood flow, which are induced by the actions of various inflammatory mediators