Novel host-modulating therapy for bacterial pneumonia


View:158 Time:2018-04-09


Dr. Hongbo Luo, a researcher at Harvard Medical School and Children's Hospital Boston, and co-workers have recently found a novel, effective way to treat bacterial pneumonia.

Bacterial pneumonia is an inflammatory condition of the lung caused by bacterial infection. Antibiotics are an important treatment option for bacterial pneumonia. Antibiotic treatment can effectively kill the disease-causing bacteria. However, the emergence of antibiotic resistance increases the bacterial pneumonia treatment difficulty. If the bacteria are not all be killed, the patient could get sick all over again.

Local patterns of antibiotic resistance should be taken into consideration when initiating pharmacotherapy. Antibiotic resistance refers to the ability of a microorganism to withstand the effects of an antibiotic that was once effective. The bacteria are resistant and continue to multiply in the presence of an antibiotic. Antibiotic resistance is one of the world's most pressing public health problems, casting a shadow over the medical miracles we take for granted.

To counteract the growing threat of antibiotic resistance, it is of great importance to develop host-modulating personalized therapies.

Most bacterial infections stimulate an increase in neutrophils at the infection site. Neutrophils, the most abundant type of white blood cells in most mammals, are the body's primary defense against bacterial infection. Neutrophils help internalize and kill the bacteria. However, these cells also cause tissue destruction by releasing inflammatory compounds in the process.

Dr. Luo is dedicated to elucidating the molecular mechanisms and cellular signaling pathways that control various neutrophil functions, in a hope to find ways to control the number and function of neutrophils during infection and inflammation.

Previously, Dr. Luo's team found that an enzyme called IP6K1 (inositol hexakisphosphate kinase 1) inhibits signaling by a molecule called PIP3. They demonstrated in mice that IP6K inhibition results in higher PIP3 and causes neutrophils to become more active, killing more bacteria and living longer.

In this work, the team used mouse pulmonary bacterial infection models to see how IP6K1 mediates protective and detrimental responses. The team found that disrupting the IP6K1 gene or pharmacologically inhibiting IP6K1 activity using a specific inhibitor called TNP efficiently and effectively enhanced host bacterial killing by neutrophils but reduced pulmonary neutrophil accumulation, minimizing the lung damage caused by different types of bacterial pneumonia.

Although TNP has not been tested as a drug in humans, these findings will likely to have potential applications by opening a new avenue for treating bacterial pneumonia and other infections. Inhibition of IP6K1 represents a potential strategy to enhance host defenses and simultaneously suppress neutrophil-mediated pulmonary damage in bacterial pneumonia. In a word, IP6K1 could be targeted to treat bacterial pneumonia.

You can read the full paper (Inhibition of IP6K1 suppresses neutrophil-mediated pulmonary damage in bacterial pneumonia) in the 4 Apr 2018 issue of the journal Science Translational Medicine.

The study is a collaboration of Harvard Medical School, Children’s Hospital Boston, Johns Hopkins University, Veterans Affairs Boston Healthcare System, Emory University School of Medicine in the USA, Chinese Academy of Medical Sciences and Peking Union Medical College in China.
 
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