IMMUNOLOGY TEXTBOOK - Mercury Podillya 2013

MECHANISMS OF IMMUNE DEFENSE IN BACTERIAL, VIRAL, FUNGAL, AND PROTOZOAN INFECTIONS

Features of the immunogram in certain inflammatory diseases

When patients present with Pseudomonas aeruginosa, Proteus, or Staphylococcus epidermidis, the primary findings are typically a decreased level of B Cells, T cells, and their regulatory subpopulations. In cases involving Escherichia coli or Staphylococcus aureus, alongside B-Cell deficiency, pathognomonic hyperproduction of immunoglobulin classes M and G was observed. These findings suggest that a pronounced deficiency of the main links of The Immune System promotes the proliferation of pathogenic agents within the infection focus, whereas a more favorable status of immune reactivity in the patient leads to the accumulation of non-pathogenic microflora.

A similar pattern was observed in women with acute Inflammatory Diseases of the uterine appendages. When opportunistic microflora were isolated, the predominant features were a decrease in the functional activity and count of T lymphocytes, alongside an excessive Lysozyme content. The combination of opportunistic flora with gonococci was accompanied by an excess of lysozyme, suppression of the lymphocyte blastogenesis reaction (LBR), and activation of the phagocytic function of neutrophils. Finally, opportunistic pathogens and campylobacteria caused inhibition of LBR, a reduction in T-cell levels, and hyperproduction of IgM.

In cholecystitis, The Nature of immune disorders is fundamentally different. It is manifested by the hyperproduction of major immunoglobulin classes and a deficiency in T-cell counts; as the condition worsens, the degree of impairment also increases.

In non-specific cervicitis, which serves as another example of a non-specific infection, patients exhibit decreased levels of T cells and B lymphocytes, along with Excessive production of IgA of the minimal first degree, indicating an imbalance in the immune system. Soft tissue pyogenic infection causes predominant changes in other marker indicators—such as LBR (PHA); the pathological process suppresses the functional activity of T cells, increases the proportion of B lymphocytes, and inhibits the count of T helpers.

In Pyelonephritis, both calculous and non-calculous variants lead to a fundamentally different form of immune disorders. Specifically, in the first case, changes affect the T-cell and phagocytic links, while In the second, they involve the T- and B-cell immune mechanisms.

Specific infection—Viral Hepatitis A—leads to a differential Immune Response depending on the severity of the disease and the presence or absence of gastroduodenitis. In atypical anicteric and mild forms, the pathological process impacts T cells, their regulatory subpopulations, and B lymphocytes, whereas in moderate and severe forms, it affects these same cells alongside natural killers.

In campylobacter dysbiocenosis, stimulation of B cells is observed alongside a decline in the levels of T suppressors and T helpers. It remains difficult to determine what is primary: whether The formation of specific immune disorders triggers The Development of dysbiosis, or whether dysbiosis dictates the Nature of the immune alterations.

In the carriage of pathogenic staphylococci on the nasal mucosa, the predominant findings were a 2nd-degree deficiency in IgG concentration, total lymphocytes, and T cells. In post-appendectomy patients, the immunological profile shifts, reflecting decreased IgG production, an excessive amount of IgM, and a deficiency in total lymphocytes.

Immune alterations in frequently ill children. Examination of cellular and humoral Immunity parameters in frequently ill children reveals fairly uniform deviations from normal values. Primarily, There is a drop in total T-lymphocyte counts, T helpers, a decreased concentration of secretory IgA, low lysozyme activity in nasal secretions, and reduced interferon-producing capacity of leukocytes. However, depending on the presence of concomitant pathology, Specific features of immune disorders emerge upon analyzing their profile.

Thus, in frequently ill children without concomitant pathology and with allergies, the cellular link of immunity is predominantly affected, manifested by a decrease in the counts of T helpers, active T cells, and T suppressors. In children with ENT disorders and tuberculosis infection, an imbalance of the T-cell link develops, as evidenced by a simultaneous drop in T helpers and active T lymphocytes alongside an increased level of T suppressors.

When ENT disorders and allergies are combined, there is a decrease in the number of T helpers and T-active lymphocytes, coupled with the hyperproduction of IgM. Finally, in overweight children, the profile of immune disorders changes fundamentally: the counts of total T cells and IgA decrease.