If you have had strep throat or an ear infection, there\u2019s a good chance you received amoxicillin or penicillin to effectively kill the troublesome bacteria.<\/p>\n
These drugs, which belong to a broad group of antibiotics called beta-lactams, are commonly used to treat various bacterial infections, from urinary tract infections to pneumonia and sepsis.<\/p>\n
But beta-lactam antibiotics can\u2014and do\u2014fail, even in the absence of antibiotic resistance.<\/p>\n
Researchers at the UNC School of Medicine have pinpointed a specific protein within our immune system that interferes with the antibiotic\u2019s ability to kill bacteria. Their results are\u00a0further explained<\/a>\u00a0in a paper published in the\u00a0Proceedings in the National Academy of Sciences.<\/p>\n \u201cWe found that a major innate immune protein sequesters essential metals, which can inadvertently allow the bacteria to survive our most widely used antibiotic class,\u201d said\u00a0Brian Conlon, PhD<\/a>, associate professor of microbiology and immunology at the UNC School of Medicine and senior author on the paper. \u201cThis is an unfortunate antagonism between beta-lactam antibiotics and our immune system that may be driving clinical failure.\u201d<\/p>\n What is Antibiotic Tolerance?<\/p>\n Antibiotic tolerance poses a great risk to patients with severe and reoccurring infections, as bacteria can withstand strong doses of antibiotics.<\/p>\n About 20% of patients with MSSA (methicillin sensitive\u00a0Staphylococcus aureus)\u00a0infections treated with oxacillin die. These outcomes are tied and to antibiotic tolerance, where pathogens are able to survive the killing activity of the antibiotic for extended periods.<\/p>\n To better understand why antibiotic tolerance occurs in such commonly used antibiotics,\u00a0Conlon and his lab<\/a>\u00a0have been on a years-long mission to understand what, within our own immune system, may be interfering with antibiotic action, in addition to the pathogens themselves.<\/p>\n Beta-lactam antibiotics work by attacking the outer protective layer of bacterial cells, known as the cell wall. When antibiotics damage this layer, bacterial enzymes called autolysins begin to eat the wall, causing it to disintegrate completely and the bacterial cell to rupture. This process is what ultimately kills entire bacterial colonies and prevents further infection.<\/p>\n The Findings<\/p>\n