CXCL-8 as a signature of severe Helicobacter pylori infection and a stimulator of stomach region-dependent immune response.

Helicobacter pylori infection is involved in development of diverse gastro-pathologies. Our aim is to investigate potential signature of cytokines-chemokine levels (IL-17A, IL-1ß, and CXCL-8) in H. pylori-infected patients and their impact on immune response in both corpus and antrum. Multivariate level analysis with machine learning model were carried out using cytokines/chemokine levels of infected Moroccan patients. In addition, Geo dataset was used to run enrichment analysis following CXCL-8 upregulation. Our analysis showed that combination of cytokines-chemokine levels allowed prediction of positive H. pylori density score with <5% of miss-classification error, with fundus CXCL-8 being the most important variable for this discrimination. Furthermore, CXCL-8 dependent expression profile was mainly associated to IL6/JAK/STAT3 signaling in the antrum, interferons alpha and gamma responses in the corpus and commonly induced transcriptional /proliferative activities. To conclude, CXCL-8 level might be a signature of Moroccan H. pylori-infected patients and an inducer of regional-dependent immune response at the gastric level. Larger trials must be carried out to validate the relevance of these results for diverse populations.

IL-1 Polymorphism and Helicobacter pylori Infection Features: Highlighting VNTR's Potential in Predicting the Susceptibility to Infection-Associated Disease Development.

Genetic polymorphisms at the IL-1 cluster are associated with increased Helicobacter pylori (H. pylori)-associated disease risk in an ethnically dependent manner. Due to the corroborated role of IL-1ß in H. pylori infection progression, our aim is to depict the impact of IL1B rs1143627 and rs16944 as well as the IL1RN variable number of identical tandem repeats (VNTR) on the clinical and biological features of Moroccan H. pylori-infected patients. A total of 58 patients with epigastralgic pain were referred to the gastroenterology department for histopathological and clinical analysis. DNA extraction from antrum and fundus biopsies and PCR-RFLP were performed to detect polymorphisms. As a result, VNTR was significantly associated with IL-1ß antrum levels (p-value = 0.029), where the *1/*4 genotype showed a positive association with upregulated cytokine levels in the antrum and was clustered with H. pylori-infected patients' features and higher levels of IL-1ß in the antrum and fundus. Likewise, *1/*1 genotype carriers clustered with severe gastritis activity and H. pylori density scores along with low levels of IL-1ß in the antrum and fundus, while the *1/*2 genotype was clustered with non-infected-patient features and normal IL-1ß levels. In conclusion, VNTR might be an interesting predictor to identify patients at risk of developing H. pylori-associated pathologies.

[Granulomatous spondylodiscitis: due mainly to tuberculosis but lymphoma cannot be excluded]. / Spondylodiscite granulomateuse: surtout la tuberculose mais ne pas omettre le lymphome.

Lower back pain is due to multiple etiologies that make diagnosis difficult. Primitive spinal lymphoma is rare and its diagnosis often requires ultrasound-guided biopsy. A 30-year old man hospitalized for inflammatory lumbago evolving within the context of an impaired general condition. Phisical examination revealed pain on palpation of the L2-L3 vertebral apophysis without peripheral tumor syndrome. Laboratory tests showed an inflammatory syndrome. Morphological assessment was in favour of a spondylodiscitis. The first biopsy showed granulomatous osteitis.Clinical and radiological worsening during antibacillary treatment led to reconsider the original diagnosis and a second biopsy confirmed the diagnosis of lymphoma. The diagnosis of skeletal tuberculosis in particular spinal tuberculosis requires bacteriological or histological confirmation in order not to overlook a primitive bone lymphoma.

[Physiopathological data of Horton's syndrome]. / Données physiopathologiques de la maladie de Horton.

GREAT PROGRESS: The understanding of the physiopathology of Horton's syndrome has been made in view of the prevalence of the disease, the access to affected tissue and new molecular biology techniques. And it is now possible to specify the intricacy between the genetic, immunological and vascular components. HORTON'S SYNDROME, A GENETIC DISEASE: The preferential association of the disease with some alleles pf the HLA DR4 group has helped to emphasize the fundamental role of a few amino acids of the second hypervariable area of the HLA-DR molecule. An immunogenetic predisposition appears favourable, or even necessary, for the development of the disease. HORTON'S SYNDROME, AN IMMUNOLOGICAL DISEASE: The temporal arteries of patients presenting with Horton's syndrome are infiltrated by polymorphous inflammatory cells, fundamentally including CD4 T-cell lymphocytes, macrophages, and a few giant cells. Some CD4 lymphocytes have undergone clonal proliferation and show signs of recent antigenic recognition. A fraction of them secrete interferon gamma, which plays a crucial role in the onset, maintenance and orientation of the immunological response. The macrophages play multiple roles notably in maintaining the inflammatory reaction, but also in the destruction of certain structures of the arterial wall. HORTON'S SYNDROME, A VASCULAR DISEASE: The destruction of the arterial wall at the acute stage of the disease appears responsible, sometimes later on, for aneurismal dilatations observed on the aorta of certain patients. Moreover, intimal hyperplasia (mediated by the PDGF (platelet derived growth factor) A and B) and thrombosis (related to the inflammation) join up in reducing the arterial flow and enhancing the risk of ischemic complications during the acute stage. PATHOGENESIS, HYPOTHESES: Various candidate-antigens have been incriminated in the onset of the inflammatory reaction during Horton's syndrome. Some epidemiological and molecular studies are in favour of an exogenous antigen, possibly infectious, but no evidence has been demonstrated in the studies published. A parietal, endogenous antigen might also be at the origin of the cascade of events described during this disease.