Comparative Characteristics of the Spleen White Pulp in Experimental Models of Sepsis Caused by Different Strains of Pseudomonas aeruginosa.

We describe reactive changes in the spleen white pulp in male C57BL/6 mice with experimental sepsis induced by intraperitoneal administration of Pseudomonas aeruginosa 1840 (Pa1840) with exotoxin U gene or Pseudomonas aeruginosa 1623 (Pa1623) with exotoxin S gene. Histological analysis and morphometry revealed hypoplasia of the spleen white pulp in mice with sepsis induced by Pa1840, while sepsis caused by Pa1623 was associated with its hyperplasia; with apoptosis of white pulp cells was observed in both cases. The results attest to ambiguous nature of the reactive changes in the white pulp of the spleen in experimental sepsis models initiated by Pa1840 and Pa1623 stains.

The formation and function of tertiary lymphoid follicles in chronic pulmonary inflammation.

Tertiary lymphoid follicles (TLFs) can develop in the respiratory tract in response to infections or chronic inflammation. However, their functional relevance remains unclear because they are implicated in both protective and pathological responses. In contrast to homeostatic conditions, external antigens and damage to the lung tissue may drive TLF formation in inflamed lungs, and once established, the presence of pulmonary TLFs may signal the progression of chronic lung disease. This novel concept will be discussed in light of recent work in chronic obstructive pulmonary disease and how changes in the pulmonary microbiota may drive and direct TLF formation and function. We will also discuss the cellularity of TLFs at the pulmonary mucosa, with emphasis on the potential roles of lymphoid tissue inducer cells, and B- and T-cell aggregates, and will examine the function of key chemokines and cytokines including CXCL13 and interleukin-17, in the formation and maintenance of pulmonary TLFs.