Alimentary System

Stomach, Glandular Stomach - Infiltration, Cellular

Narrative
Comment:
The term "cellular infiltrate" is often used to describe the presence of inflammatory cells without other evidence of an inflammatory process (e.g., edema, necrosis or degeneration of cells, evidence of vascular injury). Infiltrates usually consist of lymphocytes, mast cells, or eosinophils. Lymphocytic infiltrates in the glandular stomach can be an incidental finding; they typically appear in the deep aspect of the mucosa and in the submucosa. In Figure 1 (arrow), lymphocytic infiltrates are present in the deep mucosa of the glandular stomach and in the propria of the forestomach. Eosinophils (Figure 2 and Figure 3, arrows) are recruited from the blood stream into most organs in response to eosinophil chemoattractants present in allergic and parasitic diseases and indicate a hypersensitivity reaction.

Focal collections of mast cells can occasionally be found in the submucosa of the stomach. Mast cells have been shown to contribute importantly to acute allergic reactions, late-phase reactions, and chronic allergic inflammation. Focal accumulations of mast cells in the submucosa of the gastrointestinal tract are usually considered an incidental lesion in NTP studies. Such accumulations may be confused with mast cell tumor. Focal accumulations of mast cells tend to be smaller and less well circumscribed than mast cell tumors and infiltrate between structures rather than compressing or effacing adjacent structures.
Recommendations:
The term "infiltrate, cellular" should be used when inflammatory cells are present with no other features of inflammation (e.g., edema, hemorrhage, degeneration, necrosis). Generally, infiltrates of inflammatory cells are often quite small and may not warrant a diagnosis. When diagnosed, infiltrates should be graded based on the number of cells and the total tissue area affected. A modifier should be used to indicate the specific type of cell (e.g., lymphocyte, eosinophil, mast cell).
References:

Ackermann MR. 2007. Acute inflammation. In: Pathologic Basis of Veterinary Disease (McGavin MD, Zachary JF, eds). Mosby, St Louis, MO, 101-152.

Algood HM, Gallo-Romero J, Wilson KT, Peek RM Jr, Cover TL. 2007. Host response to Helicobacter pylori infection before initiation of the adaptive immune response. FEMS Immunol Med Microbiol 51:577-586.

Abstract: https://www.ncbi.nlm.nih.gov/pubmed/17919297

Ferrero RL, Ave P, Radcliff FJ, Labigne A, Huerre MR. 2000. Outbred mice with long-term Helicobacter felis infection develop both gastric lymphoid tissue and glandular hyperplastic lesions. J Pathol 191:333-340.

Abstract: https://www.ncbi.nlm.nih.gov/pubmed/10878557

Leininger JR, Jokinen MP, Dangler CA, Whiteley LO. 1999. Oral cavity, esophagus, and stomach. In: Pathology of the Mouse (Maronpot RR, ed). Cache River Press, St Louis, MO, 29-48.

Abstract: http://www.cacheriverpress.com/books/pathmouse.htm

Park JH, Hong JJ, Park JH. 2003. Experimental infection of mice with tightly coiled spiral bacteria ("Candidatus Helicobacter suis") originating from the pig stomach. J Comp Pathol 129:54-160.

Abstract: https://www.ncbi.nlm.nih.gov/pubmed/12921721

Wedemeyer J, Galli SJ. 2000. Mast cells and basophils in acquired immunity. Br Med Bull 56:936-955.

Abstract: https://www.ncbi.nlm.nih.gov/pubmed/11359630
  • Image of infiltration cellular in the glandular stomach from a male F344/N rat in a chronic study

    Stomach, Glandular stomach - Infiltration, Cellular, Lymphocyte in a male F344/N rat from a chronic study. Lymphocytic cellular infiltrate is present in the deep mucosa of glandular stomach (arrow).

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