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. 2019 Aug 1;200(3):370–380. doi: 10.1164/rccm.201807-1361OC

Figure 1.

Figure 1.

Cell type and effector responses distributions in and around cavity. The graphs show the mean ± SEM of per kilobase per million mapped reads (RPKM) of all genes in the module at each position; “Normal” is normal-appearing lung in tuberculosis (TB), whereas “Non-TB lung” refers to the control subjects. Cavity wall positions were combined. The Kruskal-Wallis test P value (corrected for multiple comparisons) in each graph is shown for the comparison of RPKM values in control subjects without TB versus RPKM values in the different cavity positions. For RPKM comparison between control subjects without TB and normal-appearing lung tissue in patients with multidrug-resistant TB, P value was >0.2 for all comparisons. The RPKM values were higher in macroscopically normal-appearing tissue in patients with multidrug-resistant TB compared with non-TB control lung, but were highest in the cavity wall, with a precipitous decline below non-TB lung in the cavity center. However, expression of Th2 cytokine–inducible genes and LPS response were not higher in patients with multidrug-resistant TB than in control subjects. The highest RPKM values relative to control subjects were with the type II IFN (IFN-γ)–inducible genes in the cavity wall. Also notable are the increases in B cells in the cavity wall and airways. Mtb = Mycobacterium tuberculosis; NK = natural killer; Th2 = T-helper cell type 2; TNF = tumor necrosis factor.