Lamina propria, defined

The adherence mechanisms involved in Salmonella infection have been studied in great deal. Disease associated with S. enterica serovars is initiated by attachment to and invasion of hosf cells, followed by subse-quenf inflammation of the lamina propria and lymph nodes (Darwin and Miller, 1999). Several genetically defined fimbrial or piliar adhesins con-tribufe fo fhe initial attachment and the overall infection process of Salmonella. Some of fhese include t)q)e 1 fimbriae (Fim), plasmid-encoded (PE) fimbriae, long polar (LP) fimbriae, and thin aggregative fimbriae (curli). However, many ofher putative fimbrial operons have been identified within various S. enterica serovar genomes, but the expression of fhese proteins is currently undefined. 

Biopsy specimens of PAH include constrictive lesions and complex lesions. Constrictive lesions comprise medial hypertrophy and intimal thickening. Medial hypertrophy is defined as the increase in both number and cross-sectional area of the SM cells lining the walls of the pre- and intra-acinar pulmonary arteries intimal thickening implies an increased number of fibroblasts in the thin layer between a SM cell and lamina propria of the blood vessel. These changes can be seen in both IPAH and pulmonary venous hypertension. In contrast, complex lesions are considered pathognomonic for PAH. The complex or plexiform lesion consists of focal proliferation of endothelial channels consisting of fibroblasts, SM cells, and connective tissue matrix. These lesions disrupt vascular vessel wall and serve as a nidus for in situ thrombosis. 

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