The study has demonstrated that translocation of NF-κB in the epidermis and basal cells is responsible for two of the key pathological features of psoriasis, epidermal hyperplasia, and inflammation. We have postulated that translocation of NF-κB in lymphocytes, in psoriatic skin leads to NF-κB translocation in the epidermis and basal cells. NF-κB is therefore likely to be one of the key molecules in the pathogenesis of psoriasis.
Non Syndromic Hearing Loss is an important cause for hearing loss. One in 1000 newborns have some hearing impairment. Over 400 genetic syndromes have been described. Non Syndromic Hearing Loss (NSHL) can be inherited in an Autosomal Dominant, Autosomal Recessive or a Sex Linked fashion. There are several reasons why genetic testing should be done in cases of NSHL, the main reasons being for genetic screening and for planning treatment. This review describes the genes involved in NSHL and the genetic mechanisms involved in the pathogenesis of the disease.
Helicobacter pylori (H. pylori) causes gastritis, development of lymphoid follicles and later monoclonal mucosa-associated lymphoid tissue (MALT) lymphoma. We evaluated the association of tumor necrosis factor (TNF)-alpha (-308 G/A) and IL-10 (-819 C/T) gene polymorphisms with gastritis and lymphoid follicle formation. H. pylori infection was detected using modified Giemsa staining and IgG anti-CagA enzyme-linked immunosorbent assay (ELISA). One hundred and thirty patients with non-ulcer dyspepsia (NUD) and 200 healthy age-matched controls were genotyped for TNF-alpha and IL-10 polymorphisms using polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP). Subjects with IL-10 -819 T allele [patients (46.5%) versus controls (35.7%), p = 0.006, OR = 1.56, 95% CI = 1.14-2.15] were at risk of gastritis. Infection with H. pylori was more often associated with lymphoid follicles formation than its absence (46% versus 22%, p = 0.009). TNF-alpha polymorphism did not influence gastritis but patients with TNF-alpha -308 A allele carriers showed >2 fold risk of lymphoid follicle formation [presence (26%) versus absence (11.25%), p = 0.029, OR = 2.8; 95% CI = 1.09-7.08]. There was a trend towards association of lymphoid follicles and TNF-alpha -308 A allele carriers with H. pylori infection than without (58.5% versus 22.2%; p = 0.064). IL-10 -819 T and TNF-alpha -308 A alleles may increase risk of gastritis and lymphoid follicle formation.
The role of mast cells and eosinophils in influencing the pathology of chronic gastritis remains unclear. We attempted to study the relationship between endoscopy and the mast cell and eosinophil infiltrate. We also studied the role of gene polymorphisms, Helicobacter pylori density and the CagA antibody status in influencing the mast cell and eosinophil infiltrate. One hundred and twenty consecutive patients were studied. Endoscopic evaluation was done and 3 antral biopsies were taken from each patient and were assessed for eosinophilic and mast cell infiltration, H. pylori density and the density of the other inflammatory cells as per the revised Sydney system. Cytokine gene polymorphisms (IL-1beta, IL-1RA and TNF-alpha) were done on the DNA extracted from the peripheral blood by PCR-RFLP. ELISA was done on the patients' serum for the anti-CagA antibody titres. Nodularity is strongly associated with the presence and density of eosinophils on biopsy (P < 0.05). Eosinophil density is strongly associated with the density of H. pylori, neutrophils, lymphocytes, plasma cells, atrophy, ulceration, foveolitis and lymphoid follicles. The mast cell density is not associated with any of the other histopathological variables. Gene polymorphisms and the CagA antibody titres have no relationship to the mast cell and eosinophil density. Eighty-one patients showed positive anti-CagA antibody titres but there was no association with the eosinophilic or the mast cell infiltrate. It is likely that eosinophilic infiltration is influenced by the H. pylori density but the CagA protein has no role to play in influencing the grade of the eosinophilic infiltrate in the Indian context. Cytokine gene proinflammatory polymorphisms have no role to play in influencing the eosinophilic or the mast cell response. It is likely that other mediators are involved in the inflammatory cell responses.
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