Trade Agreement between Bacteria, Viruses and Human Skin — A fly in the ointment 细菌、病毒与人皮的经贸协定 — 美中不足的共生

Staphylococcus is a group of Gram-positive cocci. It is named because it appears spherical (cocci) and form in grape-like clusters [1-4] under the microscope. Staphylococci live all over us, and seem to have adapted to conditions in our skin that are uncongenial to most other bacteria [1,4-6]. Considering that its numbers exceed us by multiple times, it is remarkable how little trouble we have with the relation. Only a few of us are plagued by boils, and we can blame a large part of the destruction of tissues on the zeal of our own leukocytes. We live with them for long periods without any awareness of their existence; then cyclically, for reasons not understood but probably related to immunologic reactions on our part, we sense them, and the reaction of sensing is the clinical disease, eg. suppurative inflammation of various tissues and organs, food poisoning, staphylococcal scalded skin syndrome (SSSS), toxic shock syndrome (TSS), etc.

Some bacteria are only harmful to us when they make exotoxins or endotoxins, and they only do this when they are, in a sense, diseased themselves. The toxins of staphylococcus, diphtheria bacilli and streptococci are produced when the organisms have been infected by bacteriophage which is a kind of virus; it is the virus that provides the code for toxin. Uninfected bacteria are uninformed. When we catch impetigo it is a virus infection, but not of us. Virus (bacteriophage) infects Staphylococcus, then staphylococci release toxins and enzymes to fight the bacteriophage (virus). When we sense toxins and enzymes released by staphylococci, we are likely to turn on every defense at our disposal; we will decapitate, bomb, defoliate, blockade, seal off, and destroy all the tissues in the area. Our soldier cells (leukocytes) become more actively phagocytic, release lysosomal enzymes, turn sticky, and aggregate together in dense masses, occluding capillaries and shutting off the bleed supply. Complement is switched on at the right point in its sequence to release chemotactic signals, calling in leukocytes from everywhere. Vessels become hyperreactive to epinephrine so that physiologic concentrations suddenly possess necrotizing properties. Pyrogen is released from leukocytes, adding fever to hemorrhage, necrosis, and shock. We are completely out of order.

Our involvement is not that of an adversary to bacteria or virus in a straightforward game, but more like blundering into someone else’s accident, it seems that the two creatures of China and the United States that were originally friendly and symbiotic on the host earth’s biosphere suddenly turned their heads and erupt into violent warfare. In real life, however, even in our worst circumstances we have always been a relatively minor interest of the vast microbial world. Pathogenicity is not the rule. Indeed, it occurs so infrequently and involves such a relatively small number of species, considering the huge population of bacteria on the earth, that it has a freakish aspect. Disease usually results from inconclusive negotiations for symbiosis, an overstepping of the line by one side or the other, a biologic misinterpretation of borders [7].

Staphylococcus4
葡萄球菌(Staphylococcus)是一群革兰氏染色阳性球菌，因常常堆聚成葡萄串状而得名[1-4]。其实葡萄球菌广泛分布于自然界及人和动物的皮肤及与外界相通的腔道中[1,4-6]。大多数细菌不适合生活在人类的皮肤上，这种菌倒似乎适应了那里的条件。看着它们人口如此之众，而我们自己是这样形单影只，然而人类与它们共生相处，麻烦却如此之少，这真是奇事一桩。我们甚至根本感觉不到它们的存在。当我们的细胞出现免疫应答时，我们才感觉到它们，这种感觉反应便是临床的病症，如多种组织器官的化脓性炎症、食物中毒、烫伤样皮肤综合征、毒性休克综合征等疾病。

这些细菌只是在产生毒素时才是对人类有害的，而从某种意义上说，它们只是在自身生病时才产生毒素。葡萄球菌只有在受到噬菌体（病毒）侵袭时才产生毒素和凝固酶；为生产毒素提供密码的是噬菌体，未受感染的细菌是没有获得密码通知的。我们染上了脓疱疮，那是种病毒感染，但病毒感染的不是我们，病毒（噬菌体）感染了葡萄球菌，葡萄球菌释放出毒素和酶反击噬菌体。但是我们的细胞一旦感觉到了葡萄球菌释放的酶和毒素，我们就可能动用一切可用的防御手段。我们的免疫系统会采取一系列军事行动斩首、轰炸、堵截、封锁，直到毁掉那一地区的所有组织。士兵们(白血球)活跃起来了，变得更具吞噬性，释出溶菌酶，变得粘稠，成群密集在一起，堵住毛细血管，切断血液供给。血清防御素司机而动，释放趋化性信号，从全身召集白细胞。血管变得对肾上腺素过度敏感，于是，生理上的集中反应突然具有了使组织坏死的性质。白细胞中放出发热原，又在出血、坏死和休克之上加上发烧。一切全乱套了。

我们卷入的不是一场跟细菌或病毒的直接对抗赛，而好像是在宿主地球生物圈上本来友好共生的中国美国两个生物突然翻脸打了起来，我们无意中撞入了他人的麻烦。然而，在现实生活中，即使在最坏的情况下，我们也从来都只是那个庞大的细菌王国相对漠不关心的对象。细菌致病并非常见，实话实说，细菌致病是这样的罕见，鉴于地球上细菌的家口之众，致病菌的种类相对来说如此稀少，这件事有着捉摸不透的一面。刘易斯·托马斯医生看透了这个生物世界，疾病是为共生而进行的谈判无结果造成的，是共生双方中的一方越过了边境线，是生物界里边界协定的误解[7]。

 

Reference:

  1. Guoqing Xia and Christiane Wolz. Phages of Staphylococcus aureus and their impact on host evolution. Infection, Genetics and Evolution. Volume 21, January 2014, Pages 593-601
  2. H.W. Ackermann. Classification of the bacteriophages of Gram-positive cocci: Micrococcus, Staphylococcus, and Streptococcus. Pathol. Biol. (Paris), 23 (1975), pp. 247-253
  3. T. Bae, T. Baba, K. Hiramatsu, O. Schneewind. Prophages of Staphylococcus aureus Newman and their contribution to virulence. Mol. Microbiol., 62 (2006), pp. 1035-1047
  4. C. Baptista, M.A. Santos, C. Sao-Jose. Phage SPP1 reversible adsorption to Bacillus subtilis cell wall teichoic acids accelerates virus recognition of membrane receptor YueB. J. Bacteriol., 190 (2008), pp. 4989-4996
  5. A. Belley, M. Callejo, F. Arhin, M. Dehbi, I. Fadhil, J. Liu, G. McKay, R.Srikumar, P. Bauda, D. Bergeron, N. Ha, M. Dubow, P. Gros, J. Pelletier, G. Moeck. Competition of bacteriophage polypeptides with native replicase proteins for binding to the DNA sliding clamp reveals a novel mechanism for DNA replication arrest in Staphylococcus aureus. Mol. Microbiol., 62 (2006), pp. 1132-1143
  6. J. Chen, R.P. NovickPhage-mediated intergeneric transfer of toxin genes Science, 323 (2009), pp. 139-141
  7. Lewis Thomas. The lives of a Cell: Notes of a Biology Watcher.Publisher, Penguin Books, 1978. P55