Some papers which have used flow cytometry to investigate innate immune cell recruitment, including neutrophils, inflammatory monocytes and monocyte-derived cells, in response to Leishmania inoculation into the mouse ear dermis (e.g. Ribeiro-Gomes et al. 2012 (PLoS Pathogens) with L. major and Thalhofer et al. 2011 (Infection and Immunity) with L. infantum), observe an increase in innate cell populations beginning at 1 or 2 weeks post-infection - after the initial infiltration during the first few hours/days.
Do the innate cells in this ‘second wave’ of infiltration function the same as in the initial infiltration? And why is there a marked decrease in the number of cells in these populations before this second wave? Differences in chemokines?
There is an excellent review by Charles Mills (CMills.Cr.Rev.Imm.2012 available on Research Gate) that may address your question. I will not compete with this detailed manuscript by summarizing an answer to your question. Please see: https://www.researchgate.net/profile/Charles_Mills2/
With respect to a second wave of neutrophil infiltration, as this occurs ‘later’ in infection, perhaps there are differences in the sources of recruitment signals. For example, during the first wave (less than 24 hours post-infection) chemokines such as IL-8 are produced at the site of infection (as has been shown by many groups), but mediators from the adaptive immune response may be responsible for the recruitment of neutrophils during the late phase of infection. Has anyone shown this?
I also think that the case of two waves of Langerhan cells, short-term and long-term, by Seré et al. 2012 (Cell) is interesting, as it highlights distinct developmental pathways of the cells in these waves.
Dear Amy,
did you check the types of macrophages infiltrated there?? In the first wave they might have a classically activated type 1 macrophage stimulated by specific set of cytokines (primarily Th1 type) whereas in second phase chemokine driven alternatively activated macrophages are coming??