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Interview: Stephen P. Diggle

Sept. 6 , 2010

World Sci­ence asked lead­ing mi­cro­bi­ol­o­gist Ste­phen P. Dig­gle to com­ment on a study on “back­stab­bing bac­te­ria” re­ported in World Sci­ence and pre­sented Sept. 6 at the fall meet­ing of the So­ci­e­ty for Gen­er­al Mi­cro­bi­ol­o­gy in Not­ting­ham, U.K. Dig­gle, a Roy­al So­ci­e­ty uni­vers­ity re­search fel­low at Not­ting­ham Uni­vers­ity, is one of the sci­en­tists in­volved in the study and is the pro­fes­sor of its lead re­sear­cher, Ph.D. stu­dent Er­ic Pol­litt.

WS: Could you concisely de­scribe how bac­terial cells inter­act so­cially with each oth­er and how an un­der­stand­ing of this can help us to fur­ther under­stand in­fect­ious dis­ease?

Micro­bio­logist Stephen P. Dig­gle is also a bass gui­tar­ist in the cover band "Ab­bey Street."


D. : In the last 20 years, we have started to appre­ciate that bac­teria are highly inter­active and ex­hibit a num­ber of so­cial be­ha­viours. One key phe­no­me­non found in many spe­cies of bac­teria is “Quo­rum Sens­ing” or QS, which de­scribes the ac­cum­ula­tion of sig­nal mole­cules pro­duced by bac­ter­ial cells [and re­leased in­to] the sur­round­ing en­vi­ron­ment. By sens­ing when the sig­nal is at a cri­ti­cal con­cen­tra­tion, bac­ter­ial cells are able to work to­geth­er to coor­din­ate pro­duct­ion of da­mag­ing tox­ins and this helps the in­fec­tion to over­whelm the host. Micro­biol­ogists have made huge strides in gain­ing an un­der­standing of the gen­etic mech­anisms in­volved in such be­hav­iours, but more re­cently we have been in­terest­ed in a more Dar­win­ian approach - how do these be­hav­iours evolve and how are they main­tained in na­ture?

WS: Be­sides the in­terest that it has in its own right, would you say that this re­search could prove use­ful from the med­i­cal pers­pec­tive?

D.: Yes in­deed. A num­ber of micro­bial so­cial be­hav­iours are in­volved in bac­terial viru­lence, and we hope to put the bac­teria them­selves at work as our allies in stal­ling or pre­vent­ing in­fect­ions. These be­hav­iours are costly for bac­terial cells to per­form and are there­fore sub­ject to exploit­ation by non-coop­er­at­ing “cheats” who gain all the bene­fits from the coop­er­ation of others but pay none of the costs. Cruc­ially, when a be­ha­viour is re­lated to viru­lence, a cheat is often less viru­lent and this has bene­fits to an in­fect­ion when they spread through it. It's rather an­al­o­gous to a hu­man society when people don't pay their taxes. These people still bene­fit from taxes paid by others but to an overall detri­ment to the pop­u­lation as a whole.

We hope that work in this field will trans­late into a solu­tion for the very ser­ious prob­lem posed by the growing spread of drug-resist­ant bac­ter­ia. Fi­nally, the un­der­stand­ing of these me­chan­isms could help in solv­ing the many mys­teries that sur­round bac­ter­ial in­fect­ions. For in­stance, why do some spe­cies of bac­teria rap­id­ly kill their host while others are re­la­tive­ly be­nign? Yers­i­nia pes­tis, the cau­sa­tive org­an­ism of plague, is a highly viru­lent hu­man path­o­gen, while the close­ly re­lated Yer­si­nia pseudo­tub­ercu­losis causes a much less se­vere di­sease.

WS: Could you in­di­cate an in­fec­tion where re­search on mo­lec­u­lar tech­niques de­vot­ed to in­flu­enc­ing bac­te­ri­al be­hav­iour could help in terms of med­i­cal treat­ment?

D.: I men­tion one in par­tic­u­lar, both for its clinical im­por­tance and be­cause it is one with which I am most fa­mil­iar, hav­ing worked with it for sev­er­al years. It is cyst­ic fi­bro­sis, where Pseu­dom­o­nas aerug­i­nosa is the caus­a­tive bac­te­ri­um. This same bac­te­ri­um is al­so a prob­lem in wound burns and for pa­tients who are im­muno­com­promised. In­ter­esting­ly this bac­ter­ium, which is found pretty much every­where, is almost harm­less to heal­thy peo­ple. 

WS: The implications of all this from the standpoint of biological evo­lution seem very cu­rious, at least judging from a pa­per that ap­peared just a few days ago and also reported here (Drug-resistant germs found to thelp their breth­ren through the at­tack.) This sto­ry, about “un­selfish” germs stud­ied by a group head­ed by James Col­lins of Bos­ton U., de­scribes bac­te­ri­al strate­gies quite dif­fer­ent from, if not di­rectly op­po­site, the ones used by the “back­stab­bing” cells of Mr. Pol­litt’s pa­per. 

D.: They are not as dif­ferent as you might think. The recent Nature paper de­scribed how a small po­pu­lation of anti­biotic-re­sist­ant cells (which they describe as al­tru­istic) could help to pro­tect a larg­er pop­u­lation of sen­si­tive ones. Mr. Pol­litt's study shows how self­ish cheats can ex­ploit tox­in pro­duct­ion to the detri­ment of the bac­terial pop­u­lation. How­ever, you could also sug­gest that the altru­ists in the Nature paper were ac­tual­ly be­ing ex­ploited by cheats. The im­port­ant point here is that under­standing the precise nature of the inter­action be­tween cells is im­port­ant to fully under­stand the bio­logy of in­fect­ions. Fu­ture work on the evo­lu­tion­ary as­pects of bac­terial be­hav­iours will help to com­ple­ment the amaz­ing body of work that has al­ready been un­der­taken at the mole­cular level and hope­fully lead to the de­velop­ment of new ways to treat infect­ion.


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World Science asked leading microbiologist Stephen P. Diggle to comment on the study on “backstabbing bacteria” reported in World Science this week and presented at the fall meeting of the Society for General Microbiology held in Nottingham, U.K. Sept. 5. Diggle, a Royal Society university research fellow at Nottingham University, is one of the scientists involved in the study and is the professor of its lead investigator, Ph.D. student Eric Pollitt. WS: Could you concisely describe this new field of molecular study, the interactions of microorganisms in infectious diseases? D.: In the last twenty years, we have started to appreciate that bacteria are highly interactive and exhibit a number of social behaviours. Microbiologists have been gaining an understanding of the molecular mechanisms involved in these behaviours – as revealed by the progress or regress of an infection – and the underlying genetic regulation. The key phenomenon here is ‘Quorum Sensing” or”QS,” the threshold where the accretion of molecular signals from the bacteria working in coordination and the consequent release of their toxins reaches a critical point, and the infection overwhelms their host. WS: Besides the interest that it has in its own right, would you say that this research could prove useful from a medical perspective? D.: Yes indeed. Many of these microbial behaviours are involved in bacterial virulence, and we can hope to put the bacteria themselves at work as our allies in stalling or preventing infections. Also, we think that work in this field will translate to progress toward the solution of the very serious problem posed by the growing spread of drug-resistant bacteria. Finally, the understanding of these mechanisms could help in solving the many misteries that surround bacterial infections. For instance, why do some species of bacteria rapidly kill their host while others are relatively benign? Yersinia pestis, the causative organism of plague, is a highly virulent human pathogen, while the closely related Yersinia pseudotuberculosis is a much less severe disease. WS: Could you indicate an infection where research on molecular techniques devoted to influence bacterial behaviour could help in terms of medical treatment? D.: I mention one in particular, both for its devastating importance and because it is one with which I am most familiar, having worked with it for several years. It is cystic fibrosis, where Pseudomonas aeruginosus is the causative bacterium. This same bacterium is also a problem in wound burns. Yet this bacterium is inoffensive in healthy people, which makes it even more intreresting. WS: Do these bacterial behaviours have implications from the social and ecological standpoints? D.: Certainly, even though we cannot say we know very much about them. WS: These implications, too, seem very curious, at least judging from a paper that appeared only a few days ago in Nature magazine and that we also publish in this page under the title “Drug-resistant germs found to thelp their brethren through the attack.” This story, about “unselfish” germs studied by a group headed by James Collins of Boston U., describes bacterial strategies quite different from, if not directly opposite, the ones used by the “backstabbing” cells of Mr. Pollitt’s paper. D.: Well, as I said we do not yet know much of the evolutive implications. In any case one cannot see a contradiction between results here, as they seem quite compatible when considering short-term vis-a-vis long-term strategies, and strategies in reference to local groups of bacteria vis-a-vis the general population. But there has been too little empirical evidence testing these theories up to now, and communication between the field of microbiology and the study of social evolution has been insufficient. The more these two fields will cooperate, the quicker will be our progress in understanding these all-important bacterial phenomena.