The Hunger Games

by Elio

I am not usu­ally drawn to start out an ar­ti­cle by con­sid­er­ing a bacterium's name, but when con­front­ed with Ag­gre­ga­ti­bac­ter ac­ti­no­my­ce­tem­co­mit­ans, I had to take a pause. A well-trav­eled Gram neg­a­tive coc­cobacil­lus, this car­rier of such a con­vo­luted moniker started life sim­ply as an Actino­bacillus iso­lated to­gether with an Actin­o­myces, later to be called a Haemophilus. It has been iso­lated from cases of bac­te­r­ial en­do­cardi­tis and ag­gres­sive pe­ri­odon­ti­tis. A de­tailed study that used mod­ern tax­o­nomic tech­niques pro­posed plac­ing this or­gan­ism in a new genus, Ag­gre­gat­i­bac­ter from the Latin, 'ag­gre­gare', to ag­gre­gate, and in a new species, actin­o­mycetem­comi­tans, from the Latin 'comi­tans', ac­com­pa­ny­ing (actin­o­mycetes). Let's call it Aa.

Graph­i­cal ab­stract of Ozuna et al. (2021) Source. Fronti­spiece: Ag­gre­gat­i­bac­ter ac­ti­no­my­ce­te­mco­mi­tans colo­nies de­velop a star-shaped struc­ture af­ter pro­longed in­cubation. Source

A re­cent study by Ozuna, Uri­arte, and De­muth (just 3 au­thors!) en­larges on their pre­vi­ous find­ing that Aa ac­quires its needed iron by ac­ti­vat­ing a two-com­po­nent quo­rum-sens­ing sys­tem, QseBC. This ac­ti­va­tion de­pends on the pres­ence of cat­e­cholamines, point­ing to a cu­ri­ous in­ter­play be­tween phar­ma­col­ogy and mi­cro­bi­ol­ogy. Where do these phar­ma­co­log­i­cally ac­tive com­pounds come from? Inter­est­ingly, they are made by neu­trophils, which are present in large amounts in in­fected sub­gin­gi­val pocket. Neu­trophils make the three main cat­e­cholamines, the well-known hor­mone ep­i­neph­rine (aka adren­a­line), plus nor­ep­i­neph­rine and dopamine. Aa in­duces the re­lease of cer­tain neu­trophil gran­ules (the so-called azurophilic ones) in which epine­phrine is stored. Of note, the QseBC sys­tem is ap­par­ently also func­tional in E coli, in­clud­ing its stim­u­la­tion by ep­i­neph­rine.

How does Aa in­ter­act with ep­i­neph­rine? Us­ing mu­tants in the QseBC two com­po­nent sys­tem, the au­thors de­ter­mined that the cy­to­plas­mic do­main of the QseC sen­sor ki­nase is needed for the in­teraction be­tween Aa and ep­i­neph­rine. Be­yond that, ep­i­neph­rine-con­tain­ing su­per­natants from hu­man neu­trophils pro­mote the growth of Aa and, un­der anaer­o­bic con­di­tions, in­duce the ex­pression of the qseBC operon. The au­thors con­clude: "The pre­sented find­ings sup­ply ev­i­dence to­wards the grow­ing field of mi­cro­bial en­docrinol­ogy by con­tribut­ing to the un­der­stand­ing of the crosstalk be­tween bac­te­ria and the host en­docrine sys­tem. Fur­ther­more, it ex­pands the know­ledge of the role of stress hor­mones in pe­ri­odon­tal dis­ease and po­ten­tially other chronic inflam­matory dis­eases."

The ar­ti­cle was pointed out to me by my friend and in­fec­tious dis­ease ex­pert Joshua Fierer. He said: "That neu­trophils syn­the­size ep­i­neph­rine got me to think­ing about what func­tion that might have for the host. Neu­rophils have such lim­ited syn­thetic ma­chin­ery, why make and re­lease epi­nephrine when they are do­ing bat­tle? Got me to spec­u­lat­ing whether this is a way of con­strict­ing blood ves­sels to keep the in­vader lo­cal­ized. Some­one should mu­tate the neu­trophil path­way to see what hap­pens."

 

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