Fig. 7: Post-resolution PGE₂ via EP4 determine re-emergence of memory T cells in response to secondary infection.

A Minipumps loaded with either the pan COX inhibitor naproxen or the EP4 antagonist MF498 were implanted into mice post-resolution four days after intranasal S. pneumoniae. 6 weeks after the initial challenge (or 38 days after this intervention), these sensitised mice or their controls were challenged with S. pneumoniae and impact of this intervention on (B) CD4⁺/CD44⁺/CD62L⁺ and (C) CD4⁺/CD44⁺/CD62L^-/CD27⁺ T cell numbers was determined 24 h later. Indeed, levels of expression of (D) CD103 and the T cell activation markers (E) CD69 and (F) CD44 was also determined on CD4⁺/CD44⁺/CD62L^-/CD27⁺ T cells. Besides lymphocytes we determined how inhibition of PGE₂ synthesis or EP4 antagonism also impacted on the ability to recruit (G) neutrophils and ultimately clear the secondary challenge of (H) S. pneumoniae. Data were analysed by one-way analysis of variance (ANOVA) and Tukey’s multiple comparisons test. A p value of <0.05 was taken as the threshold of significance with graphical representation as; p < 0.05 = *, p < 0.01 = ** and p < 0.001 = *** and presented as mean ± SEM (n = 4–5 mice/group).