Inflammation, Immunity, Vaccines for Helicobacter pylori infection

Abstract

Over the last decades, it has become evident that chronic infection by Helicobacter pylori is achieved by colonizing an almost exclusive niche and hiding from many of the host's cellular immune defense mechanisms. Although recent years have seen progress in our understanding of the innate and adaptive immune response against H. pylori, it is still uncertain how to promote the development of immunity with the final goal of a successful vaccine. Research published in the last year revealed an intriguing mutual regulation of innate response mechanisms of mucosal epithelial cells by the host and H. pylori, respectively. A further focus was put on the interaction between H. pylori and dendritic cells, with some emphasis on the inflammasome and the resulting T-cell responses. Moreover, the function of microRNAs in macrophages and gastric MALT lymphoma development has been studied in more detail. Several novel antigens and adjuvants have been tested as vaccination strategies, primarily in mice. In this review, we present a concise summary of advances in the area of inflammation, immunity, and vaccines during the last twelve months.While establishing a long-lasting infection, Helicobacter pylori deals with several obstacles of host defense, the harsh stomach environment with its very low pH and sticky mucus, the epithelial layer, which forms the first line of the cellular innate immune response, followed by macrophages and dendritic cells (DCs). Subsequent to the initial epithelial cell responses triggered by the infection, neutrophils and inflammatory monocytes are recruited, followed by the infiltration of adaptive immune cells, mainly T lymphocytes. Here we review recent findings of the past year highlighting the scenario of innate and adaptive immune responses induced by H. pylori.

Helicobacter pylori infection: A recent approach to diagnosis and management

“…However, the development of a successful vaccine producing immunity against H. pylori is still uncertain [88]. Anti IL-22 antibody injection efficiently killed H. pylori in an in-vitro mice model.…”

Avances en la búsqueda de la vacuna contra Helicobacter pylori

“…[17][18][19] . Al infectar la mucosa gástrica se produce un aumento local en la síntesis y secreción de citoquinas proinflamatorias como las IL (Interleucinas) 1B, 6, 8, 12, 18 y 23, INF-ƴ (Interferón-ƴ) y TNF-α (Factor de Necrosis Tumoral-α) por parte de varias células, como las células dendríticas, células T, monocitos y neutrófilos, entre otras, en respuesta a moléculas y sustancias secretadas por la bacteria y a la interacción directa con ella [20][21][22][23][24][25] .…”

“…La mayoría de estudios sobre la vacuna de H. pylori han utilizado ureasa como el antígeno inductor de la inmunidad 17 . Los resultados con su uso han sido variables dependiendo de la ruta, el adyuvante y la forma de esta proteína, pasando desde ningún efecto inmunológico o protector hasta claras seroconversiones y reducciones en la carga bacteriana que suelen oscilar entre uno y dos logaritmos [52][53][54][55] .…”

“…Varias rutas se han probado a la hora de evaluar una posible vacuna contra H. pylori 17,72,73 . La exposición al antígeno y al adyuvante a través de rutas directas al conducto gastrointestinal, como la mucosa sublingual o la vía intranasal, han sido las de mayor éxito hasta ahora 14,71 .…”

Helicobacter pylori infection reduces disease severity in an experimental model of multiple sclerosis

“…Approximately 10-15% of those infected develop symptomatic disease, including gastric or duodenal ulcers and gastric cancer (Atherton, 2006). In the vast majority of cases, however, colonization leads to asymptomatic chronic gastritis, with increased infiltration of neutrophils, dendritic cells (DCs), macrophages, natural killer (NK) cells, and lymphocytes into the gastric mucosa (reviewed in Robinson and Atherton, 2010;Koch et al, 2013). There is increased abundance of pro-inflammatory T-helper 1 (Th1) and Th17 subsets, as well as anti-inflammatory regulatory T cells (Tregs) (Lundgren et al, 2005;Robinson et al, 2008;Serrano et al, 2013).…”