{'fraction_non_alphanumeric': 0.021026894865525673, 'fraction_numerical': 0.007823960880195598, 'mean_word_length': 5.515923566878981, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Neutrophil activation and renal scarring.

To the Editor: In their recently published manuscript, Svensson et al present data that implicates dysfunctional neutrophil responses in the initiation of renal scarring [1]. Using IL-8 receptor-deficient mice they have elegantly shown that the disruption of neutrophil trafficking results in prolongation of infection, abscess formation, retention of neutrophils within the inflamed tissue, and eventually progressive renal scarring. These are important findings as they begin to address the central question of individual susceptibility to urinary tract infection, and provide a mechanistic interpretation for findings of potential IL-8 receptor deficiency states in humans [2]. What these authors fail to acknowledge is that as early as 1988 we proposed that aberrant activation of neutrophil respiratory burst activation and degranulation by type I fimbriate uropathogenic Escherichia coli was a key factor in the genesis of renal scarring [3, 4]. While the model chosen would seem to have some advantages over previous ones of ascending infection or direct injection, what the current study fails to address in these compromised animals is the relative importance of bacterial virulence versus host susceptibility in contributing to urinary tract infection (UTI) and renal scarring. These authors have long acknowledged and published widely on the importance of P-fimbriae in ascending infection and, although initially skeptical [5, 6] despite the demonstration of their expression in vivo [7], have lately accepted (without ever citing our work) the important virulence enhancing properties of MS or type 1 fimbriae [8, 9]. While the data presented in this manuscript are important, it must be accepted that these experiments are performed in a uniquely susceptible host. It will be important in future work to marry observations of host susceptibility to those on bacterial virulence, which will hopefully provide a better understanding of the pathogenesis of urinary tract and renal infection.